Medicine Review Booklet by Dr. Aryan (Medical Booklet Series by Dr. Aryan Part 19)

Medicine Review
A Free Booklet Series by Dr. Aryan

Preface:
• This is the study material designed by Dr. Aryan with creation and compilation of the
best of the best and the most finest slides on the subject. I would like to offer a billion
heartily thanks for everyone who contributed directly or indirectly to the creation of
the material through creation and dissemination of the scientific information.
• Covering everything in one study material is next to impossible. Hence, refer to gold
standard textbooks for building solid concepts or in case of any doubt. Textbooks are
acknowledged at the end of the presentation. If any source has been missed to
acknowledge, it doesn’t lessen their impact and contribution in any way.
• Don’t keep searching for pattern between the consecutive slides. You won’t find
many. Rather to boost your recall and review, I have constructed many slides and are
deliberately placed with no much relation between the preceding and the succeeding
ones.
• The main rule of a review material is that it must make you recall or learn maximum
amount of information in minimum amount of time and space.
• Motivational quotes and articles are included within the slides. Always remember
that every good idea, nice piece of information and everything else is literally and
absolutely worthless unless you execute.
• If you know everything in the slides in much detail, you probably wouldn’t need this
material.
Best of luck WORK & SUCCESS!
Dr. Aryan
(Anish Dhakal)

5 Steps of Asthma control
Dr. Aryan (Anish Dhakal)

• Inhaled steroids: 200-800 mcg/day
• High dose inhaled steroids: 2000 mcg/day.

COPD Treatment

Like the R–R interval, the QT interval is dependent on the heart rate in an obvious
way (i.e. the faster the heart rate, the shorter the R–R interval and QT interval)
and may be adjusted to improve the detection of patients at increased risk of
ventricular arrhythmia.

Diagnosis of Asthma

Smoking Index (SI): No. of cigarettes per day * No. of years smoked
i. <100 is mild
ii. 101-300 is moderate
iii. >300 is heavy smoker

Weekly upper limit for alcohol is 14 units for women and 21 units for men.

How to describe a arterial pulse?
I. Rate (best accessed by radial artery)
II. Rhythm
III. Volume (best accessed by carotid artery)
IV. Character
V. Condition of the arterial wall
VI. Radio-radial & radio-femoral delay
VII.Palpation of other peripheral arteries

Pulse deficit (Apex pulse deficit)
• difference between heart rate and pulse rate
• causes include ventricular premature beats &
atrial fibrillation
Ventricular Premature
Beats
Atrial Fibrillations
Pulse deficit is less (< 10/min) > 10/ min pulse deficit
“a” wave present in JVP Absence of “a” wave
Decreases or disappears on
exertion
Persists or increases
Short pause followed by a long
pause
Pauses are variable and chaotic

Premature Ventricular Contractions
• Couplet: Two successive PVCs
• Bigeminy: Sinus beat followed by PVC
• Trigeminy: Two sinus beat followed by PVCs

Normal pulse is catacrotic pulse. Many abnormalities are possible. Examples:
 Anacrotic pulse (pulsus et tardus): pulsus parvus means slow volume pulse
& pulsus tardus means pulse that peaks but later in systole
 Pulsus bisferiens: single pulse wave, two peaks in systole
 Pulsus dicroticus: one peak in systole, one in diastole
 Pulsus alternans: alternating small and large volume pulse
 Hypokinetic & Hyperkinetic pulse
 Water hammer pulse
 Pulsus paradoxus

What is Pulsus paradoxus?
• Decrease in blood pressure greater than 10 mm Hg on
inspiration
• Associated with cardiac tamponade, constrictive pericarditis,
severe asthma and SVC obstruction
• Normally on inspiration, there is decrease in intrathoracic
pressure resulting blood pooling in pulmonary vasculature and
right ventricle. This causes decrease venous return from lungs to
left atrium and thus less volume ejected from left ventricle.
• In pulsus paradoxus causing conditions there is further
increased pooling of blood in right atrium causing pressure in
the interventricular septum to left side and various other
mechanisms (viz. external compressing force by fluids in cardiac
tamponade while expanded lungs compress heart in severe
asthma)
Remember, Kussmaul sign (paradoxical rise of JVP on inspiration) is often associated
with constrictive pericarditis or restrictive cardiomyopathy.

Water hammer pulse is characterized by rapid upward stroke, ill sustained peak and rapid
downward stroke. Measurement is by palpating both radial and ulnar arteries at once & then
elevating the arm to let diastolic pulse fall further and note the volume change.

Normal respiration rate is 12 to 20 breaths/minute
Tachypnoea is RR> 20 & Bradypnoea <12
Hypoventilation & Hyperventilation refer to changes in depth of breathing
Hyperpnoea is increase in both rate and depth of breathing
Cheyne-Strokes breathing is alternating
hyperpnoea followed by apnea. Seen in left
ventricular or renal failure, narcotic
poisoning or raised ICP
Kussmaul’s breathing is rapid, gasping & very
deep type of breathing (air hunger).
Common in metabolic acidosis (DKA),
uremia, hepatic failure, pontine lesions
Respiration is
thoraco-abdominal
in females owing to
greater strength of
intercostal
compared to males
in which diaphragm
is stronger

Pursed lips in diseases like emphysema increases the intrabronchial
pressure above the surrounding alveoli thus preventing collapse.

Orthostatic hypotension means decrease in systolic blood pressure of
20 mm Hg or a decrease in diastolic blood pressure of 10 mm Hg
within 3 minutes of standing when compared with blood pressure
from the sitting or supine position.

Types of Fever Special Points
Intermittent fever Fever present for only few hours and touches the baseline in
between (quotidian, tertian, quartan fever)
Continuous fever Fever present continuously, fluctuation doesn’t exceed 1 degree C
and never touches the baseline
Remittent fever Fever present continuously, fluctuation > 1 degree C but never
touches the baseline
Pel-Ebstein fever Fever lasting for 3-10 days with an afebrile period of 3-10 days
Saddle back fever Fever lasting for 2-3 days followed by remission and fever
reappears and continues for 2-3 days
Camel hump fever Double spikes of fever within a single day
Step ladder fever Fever gradually spikes with step ladder pattern with each spike

Durack and Street (1995) have defined classical FUO as fever higher than 38.3°C
(101°F) lasting for > 3 weeks with 3 days at hospital or 3 out patient visits or 1
week of “intelligent and invasive” investigation, the cause still not being
elucidated.

Where to look for?
Pallor Icterus Peripheral
Cyanosis
Central
Cyanosis
Lower palpebral
conjunctiva
Upper bulbar sclera Tip of nose Inner aspect of lips
Tongue (tip &
dorsum)
Under surface of
tongue
Ear lobe Tongue (margin and
undersurface)
Nail beds Palate Outer aspect of lips Mucous membranes
of gum, palate,
cheeks
Palms & Soles Palm & Soles Palms & Soles Sites of peripheral
cyanosis
General skin surface General skin surface Tip of finger and
toes

Central Cyanosis Peripheral Cyanosis
Decreased arterial oxygen saturation
(pAO2 < 85%) either due to imperfect
oxygenation or admixture of venous and
arterial blood
Slowing of blood flow to an area
resulting in greater extraction of oxygen
from normally saturated blood
Generalized Seen in tip of nose, ear lobes, outer
aspect of lips, palms and soles, tip of
finger and toes
Associated with clubbing or
polycythemia occasionally
No such associations
Extremities are warm. No change on
application of warmth
Extremities are cold. Cyanosis
disappears on application of warmth
Saturation is low (<85%). So oxygen can
cause improvement.
Normal saturation, so no improvement
with oxygen therapy
Causes include cardiac causes (TOF,
transposition of great vessels,
Eisenmenger syndrome), lung causes (
pulmonary edema, COPD with cor
pulmonale), high altitude or abnormal
hemoglobin like methemoglobinaemia
Usually due to diminished blood flow
(mitral stenosis, CCF, shock) or
peripheral vasoconstriction (cold
exposure, Raynaud's phenomenon,
peripheral vascular disease)

Higher Mental Function
1. Orientation
2. Attention & Concentration
3. Memory
4. Intelligence (comprehension, general fund of
knowledge, calculation)
5. Abstraction
6. Judgment
7. Insight

Attributes Bulbar Palsy Pseudobulbar Palsy
Type of lesion LMN palsy UMN palsy
Emotions Normal Labile
Dysarthria Nasal speech Donald duck speech
(spastic)
Tongue Flaccid, fasciculating Spastic, small for mouth
Jaw jerk Normal or absent Increased
Other findings Associated with motor
neuron disease
UMN lesion of limbs

Absolute Contraindications to Thrombolytic
Therapy in Myocardial Infarction Patients
Prior ICH
AV malformation
Ischemic stroke within 3 months
Bleeding diathesis
Active bleeding
Intracranial neoplasm
Trauma to head within 3 months
Suspected aortic dissection
Thrombolytic therapy only beneficial for STEMI. Do not even think of giving it in NSTEMI or
unstable angina.

Nitrates in a Nutshell
Nitrates can be given for angina for a maximum of 3 times (can
also be used prophylactically). If no response to nitrates,
consider infraction.
Never ever give nitrates with patient under PDE-5 inhibitors like
sildenafil, in previously hypotensive patients and right
ventricular MI usually associated with inferior MI.
Look for signs of inferior MI viz. hypotension, increased JVP and
clear lungs.
Right ventricular infraction patients are preload dependent.
Nitrates would only worsen the condition. Treat with IV fluids if
JVP is normal. If JVP is raised, it signifies that it is already
overloaded.

Complications of MI
Recurrect ischemia
Post-infarction pericarditis (pleuritic chest pain,
improves on leaning forward, non-specific ST elevation
and pericardial friction rub)
Dressler syndrome (cardiac antigens form immune
complex in pericardium, lungs and pleura)
Papillary muscle rupture
Interventricular septal rupture
Ventricular aneurysm
Arrhythmias

Liebermeister’s Rule
For every degree Celsius rise in temperature, the
pulse rises by 8 beats per minute.
The exception to the rule is Faget’s sign (also known
as pulse-temperature dissociation.
Faget’s sign is seen with typhoid fever, yellow fever,
tularemia, brucellosis or cases of atypical
pneumonia.

Criteria for Dengue Fever
Hemorrhagic manifestations is detected by spontaneous bleeding or a positive tourniquet
test (blood pressure cuff inflated for 5 minutes at midpoint pressure between systolic and
diastolic pressures. >10 to 20 petechiae per square inch (6.25 cm2) signifies positive test
indicating capillary fragility.

Types of Typhoid Vaccines

Different from NYHA functional classification (Cumulative for Symptoms and Treatment)
Stage A: Control risk factors
Stage B: LV remodeling, prior MI or valvular disease. Use ACEI, ß-blockers and Statins
Stage C: Use ARNI (e.g. Valsartan/Sacubitril), Aldosterone antagonists, Hydralazine +
Isosorbide dinitrate, Diuretics and digoxin for symptomatic relief
Stage D: Fluid restriction (2L/day), Ventricular assist devices, Cardiac transplantation
Implantable Cardioverter Defibrillator (ICD) for NYHA II-III and EF ≤ 35 % on therapy
Heart failure with preserved ejection fraction (HFpEF) requires HTN, AF control and
diuretics if features of volume overload (crackles, rise in JVP or edema).

Confusion Corner: Hypertension Guidelines
Blood pressure goal is < 130/80 mm Hg (less strict control if > 75 years, co-morbidities or
limited life expectancy). The recommendation is by ACC/AHA. JNC 7 previously opted the
same target for DM/CKD patients and < 140/90 for all others.
JNC 8 is the opinion of writers and not the official endorsed guideline of NIH (states elderly
low risk patients to be started on therapy if bp > 150 mm Hg). Recent SPRINT trial showed
that high risk individuals aged 50-80 years could benefit from lower targets of <120/80 mm
Hg.
Lifestyle Modification must always be emphasized with or without drugs (Exercise, DASH
diet, Potassium supplements, Reduce salt intake, Limit alcohol, Quit smoking)
Stage 1 (Systolic: 130-139 or Diastolic: 80-89) & Low risk patients: Lifestyle modifications
Stage 1 (Systolic: 130-139 or Diastolic: 80-89): & High risk patients: Thiazide, ACEI or ARB
or CCB. Switch classes if not controlled.
Stage 2 (Systolic: ≥ 140 or Diastolic ≥ 90) : Medications similar to Stage 1. If already ≥
150/90 mm Hg, start combination therapy. If not controlled:
i. Check compliance
ii. Switch to more suitable class (ACEI/ARB for DM, ß-blocker for HF) or add a 3rd agent
iii. Suspect resistant HTN/Secondary hypertension
iv. Treat cause. Initiate Spironolactone, Eplerenone; Labetalol, Carvedilol, Hydralazine,
Clonidine.

ACE Inhibitors/ARBs Role in Efferent Arteriole
ACEI and ARBs prevent constriction of efferent arteriole thus
dilating it (Remember, NSAIDs act on afferent arteriole by
inhibiting prostaglandins formation and thus constricting it).
Either ways both medications can precipitate acute kidney
injury.
In bilateral renal artery stenosis which is a cause of CKD, the
dilation of efferent arteriole by the use of ACEI/ARBs can
decrease glomerular pressure, increase creatinine and
decrease GFR.
In practice, most patients with bilateral renal artery stenosis
can fairly tolerate the therapy but should always be monitored
closely for possible AKI.

Confusion Corner: Distributive (Warm) Shock
Primary pathology is peripheral vasodilation leading to decreased systemic vascular resistance
(SVR) and low blood pressure causing problem in distribution even though heart is normal.
Peripheral vasodilation causes fast capillary refill and warm, well perfused extremities (though
in later stages blood may be diverted to vital organs mimicking other three types of shock).
Septic shock, anaphylactic shock and neurogenic shock are the major subtypes.
Parameters in pulmonary catheterization (Swan-Ganz catheter) are different than the other three:
A. Cardiac index (CI): Normal to increased (Exception: Neurogenic shock). Decreased in other
three. Can be normal in initial stages of hypovolemic shock
B. Systemic Vascular Resistance (SVR): Decreased (Increased in other three types of shock)
C. Pulmonary Capillary Wedge Pressure (PCWP): Normal or decreased (Increased in
cardiogenic, decreased in hypovolemic, increased or decreased as per individual cause in
obstructive)
D. Mixed Venous Oxygen Saturation (SvO2): Increased (Decreased in other three types of shock)
Fever, left shift with leukocytosis (Bandemia), increase lactate may indicate septic shock while
bradycardia in the setting of shock points towards neurogenic etiology.
Mainstay of management is IV fluids. Use vasopressors as needed. Careful to exclude
cardiogenic and obstructive shock as excess IV fluid might cause fluid overload (Exception is
right ventricular infarction causing cardiogenic shock: preload dependent).

What is S1Q3T3 pattern (McGinn-White Sign)
on ECG?
Large S wave in lead I
Q wave in lead III
Inverted T wave in lead III
Seen in some cases of pulmonary embolism. However, the
most common ECG finding in pulmonary embolism is sinus
tachycardia.
Together three changes in ECG denote right heart strain.
May also signify other causes of acute cor pulmonale viz. ARDS,
acute bronchospasm or pneumothorax.

Confusion Corner: Chest X-Ray AP View
Most of the Chest X-Ray you see would
be in PA view but that doesn’t mean
that you should fall silent when other
views of X-Ray are presented.
Features of AP view:
Scapula shadow in the lung field
Heart is magnified
Ribs are more or less parallel
Vertebrae behind cardiac shadow
is clearly visible
Superior mediastinum is widened

What do you understand by P Mitrale?
The width of P wave is more than 3
small squares (> 0.12 seconds) and
notched (somewhat M-shaped). The
gaps between two peaks is greater than
0.04 seconds (1 small square)
The pathophysiology behind this is
really simple. Since P mitrale is
classically seen in left atrial
enlargement, it takes more time to
depolarize the enlarged left atrium
compared of the right atrium. Hence,
the notched appearance.
P pulmonale: right atrium enlargement: P
wave amplitude (height) > 2.5 mm (>0.25
millivolts)

Left Axis Deviation Causes Right Axis Deviation Causes
WPW syndrome can cause both left or right axis deviation
Left ventricular hypertrophy Right ventricular hypertrophy
Ostium primum ASD Ostium secundum ASD
Inferior MI Anterolateral MI
Left anterior hemiblock Left posterior hemiblock
Chronic lung disease
Pulmonary embolism

How do you diagnose LVH on ECG?
Voltage criteria (most commonly used Sokolov-
Lyon criteria):
S-wave depth in V1 + R-wave height in V5/V6 >35
mm
Non-voltage criteria:
R-wave peak time >50 ms in V5/V6
ST segment depression & T wave inversion in left
sided leads (Left ventricular strain pattern)

Bundle Branch Blocks Decoded

Two classic ECG finding in Wolf Parkinson
White Syndrome?
A. Short PR interval
(<120 ms)
B. Delta wave (slurred
upstroke of the QRS
complex)

Trigeminal Nerve Examination in a Nutshell
Sensory Examination Motor Examination Reflexes Examination
 Ask the patient to close
the eyes
 Test for sensation (light
touch, temperature
and pain) over
forehead, cheeks and
mandible comparing
both sides
 Inspect for symmetry of
temporal fossa and jaw
 Ask to clench teeth
then feel over the
masseter and
temporalis
 Ask to open and close
mouth against
resistance to test the
pterygoids
 Corneal reflex: Ask the patient to
look towards opposite site. Touch
lateral edge of cornea with light
whisp of cotton. Watch for
blinking on both sides (consensual
reflex on other eye). Also tests
facial nerve (CN 7): efferent
component. In addition, perform
Schirmer’s test for secretory
function and stapedial reflex for
facial nerve.
 Jaw jerk reflex/Masseter reflex:
Place your index finger over chin
and tap with knee hammer with
mouth slightly open. Normally
absent or very slight. Quite
pronounced in UMN lesions.

Vagus Nerve Tests in a Nutshell
i. Gag reflex (touch posterior pharyngeal wall with swab stick
causing contraction of pharyngeal and palatal muscles):
Afferent: CN 9 and Efferent CN 10
ii. Ask patient to say “aah”: elevation of soft palates on both
sides with central uvula
iii.Touch each side of palate with swab stick (contraction of
ipsilateral half of palatal muscles with deviation of uvula
towards that side): Afferent: CN 5 & CN 9 and Efferent: CN 10
iv.Observe and listen for hoarseness, stridor, any respiratory
distress especially suprasternal suction (recurrent laryngeal
nerve: branch of vagus). Laryngoscopy to look for movement
of vocal cord.
v. Two additional tests for completion: Oculocardiac reflex
(slowing of heart on orbital compression) & Carotid reflex
(slowing of heart rate and lowering of blood pressure on
stretching of carotid sinus).

Spasticity denotes speed dependent increase in tone better appreciated when passive
movement is carried out rapidly in contrast to rigidity which means sustained resistance
throughout the range of motion better appreciated when the limb is moved slowly.

Plantar reflex (L5, S1) in a Nutshell
Normal response: Plantar flexion of foot and toes along with adduction of
toes. Contraction of tensor fasciae lata, flexion and inversion of foot may
also be present.
Abnormal extensor plantar response (Babinski’s sign): Dorsiflexion of
great toe, extension and fanning of other toes, dorsiflexion of ankle and
flexion withdrawal of knee and hip. Dorsiflexion of the toes might be the
only visible effect in most cases but contraction of leg and thigh muscles can
be detected by palpation. Contraction of tensor fasciae lata has been
termed Brissaud’s reflex.
Can be normal in infancy, deep sleep, deep anesthesia, narcotic overdose
or alcohol intoxication, following ECT or coma due to metabolic
disturbances.
Other methods for eliciting plantar reflex exists (apart from scratching the
border of sole from heel to 2nd metatarsus):
Oppenheim reflex (Skin-toe reflex): apply heavy pressure by thumb and
index finger to anteromedial surface of tibia from above downwards
Gordon’s sign (Calf-toe sign): squeeze or pinch calf muscle or Achilles tendon
Shaefer’s sign: squeeze or deep pressure on Achilles tendon
Chaddock sign: strike around lateral malleolus in circular fashion

Hoffman’s & Rossolimo’s reflex
Hoffman’s reflex: With patient hand dorsiflexed
and fingers partially flexed, flick the terminal phalanx
of the patient’s finger downwards. Positive sign is seen
if thumb flexes and adducts along with other fingers
(cortical lesion is possible).
Rossolimo’s reflex: Percussion at the tip of toes
leads to exaggerated flexion of toes in pyramidal tract
lesions.

Examination of Clonus in a Nutshell
The goal is to stretch the already hypertonic muscles
suddenly and maintaining the stretching during relaxation
phase. Clonus continues unless you remove the stretch
stimulus.
Ankle clonus: With knee and hip slightly flexed, suddenly
dorsiflex the ankle. Clonus up to 5 beats can be physiological
as well. If greater than 10 beats, it’s termed as sustained
clonus. Clonus can be documented as grade 5 or just 4
(highest grade of the reflexes) while evaluating reflexes.
Patellar clonus: Holding the patella between thumb and
index finger, suddenly move the patella downwards.

Superficial
sensation
Deep or Proprioceptive
sensation
Cortical
sensation
Pain Joint sense One point (tactile)
localization
Touch Position sense Two point
discrimination
Temperature Vibration Astereognosis
Graphaesthesia
Sensory Examination in a Nutshell

What do you understand by Ortner’s
syndrome?
Ortner’s syndrome is the development of
unilateral vocal cord palsy secondary to
cardiovascular disease.

Can you expect hemoptysis in a case
of Mitral Stenosis?
Yes
In mitral stenosis are secondary to decreased
blood flow over the valve causes left atrial
pressure to rise with subsequent congestion and
increased pressures in the pulmonary circulation.
Hemoptysis, though less common is due to
increased pressures causing rupture of pulmonary
vessels.

Can you name a cause of secondary
hypertension diagnosed by Chest X-Ray and
Barium meal?
Coarctation of aorta
Notching of ribs, Figure of 3 in Chest X-Ray
Reverse 3 or E sign in Barium meal

Peripheral Signs of AR

What is Coronary Steal Phenomenon?
Never ever to be confused with Subclavian Steal Syndrome
The phenomenon occurs when there is prior narrowing of the
coronary arteries
Narrowed arteries are already dilated in order to maintain the
supply to the ischemic or less perfused areas
When powerful vasodilators is administered, the dilation
occurs in normal vessels instead of already maximally dilated
vessels further worsening the ischemia
Dipyridamole is the classic. Other vasodilators like hydralazine,
nitroprusside, isoflurane anesthetic, acetylcholine and
adenosine can also exhibit the phenomenon to varying degrees
The worsening of ischemia, symptoms and ECG findings forms
the basis of many pharmacological cardiac stress tests

Watershed areas in Colon prone to Ischemic colitis
Patients particularly at high risk are those with atherosclerotic vascular disease
whose hospital course is complicated by hypotension due to increased
perioperative fluid loss or excessive use of diuretics. Presentation usually involves
acute onset of lower abdominal pain followed by bloody diarrhea along with fever,
nausea, vomiting and leukocytosis. X-Rays are not diagnostic but may show
thumbprint sign secondary to large bowel thickening.

Carcinoid Syndrome in a Nutshell
Classic triad includes flushing, diarrhea and cardiac
involvement.
As a paraneoplastic syndrome particularly in tumors with
hepatic metastasis. Much less likely in isolated tumors without
metastasis.
5-hydroxytryptophan is degraded in liver to 5-hydroxyindole
acetic acid (5-HIAA).
Serotonin (5-hydroxytryptamine) is synthesized from
tryptophan.
Tryptophan is also a precursor of Vitamin B3 (Niacin). More
tryptophan utilized for serotonin formation would place the
person at the risk of niacin deficiency (Pellagra and its 4 D’s:
Diarrhea, Dermatitis, Dementia and Death).
Surgery is the mainstay for the tumor. If carcinoid tumors are
advanced and cannot be removed surgically, treatment of choice
is octreotide.

Mallory-Weiss tear Boerhaave syndrome
Mucosal tear secondary to forceful
retching with submucosal arterial or
venous plexus bleeding
Esophageal transmural tear with air/fluid
leakage into nearby areas
(pleura/mediastinum)
Epigastric pain, vomiting, retching,
hematemesis
Severe epigastric and low sternal pain of
sudden onset followed by fever,
leukocytosis and very sick-looking patient.
Dyspnea, odynophagia and features of
septic shock can be seen. Subcutaneous
emphysema may also be seen.
Esophagogastroduodenoscopy (EGD)
confirms the diagnosis
CT or contrast esophagography with
gastrografin confirms diagnosis.
Chest X-Ray may show pleural effusions
and pneumomediastinum. Pleural fluid if
analyzed shows a exudative fluid with very
high amylase.
Endoscopy therapy is preferred if
tear doesn’t heal spontaneously
Surgery is needed for thoracic perforations.
Conservative therapy is enough for cervical
perforations.

What do you mean by TPN gall stones?
Yes, you heard that right. Normally the presence of
proteins and fatty acids in the duodenum acts as a
stimulus for release of cholecystokinin (CCK) to
stimulate the contraction of gallbladder.
In patients with total parenteral nutrition or
prolonged fasting, normal stimulus for CCK is absent.
This leads to increased biliary stasis and formation of
bile sludge or gall stones.
If enterohepatic circulation is decreased by any
means, it would be an additional risk factor for gall
stone formation.

SAAG (Serum Ascites Albumin Gradient)
SAAG >1.1 g/dL means increased portal pressure.
Many students confuse value >1.1 with liver related
ascites. This is not true as conditions like heart failure
or constrictive pericarditis can cause ascites with high
gradient. Liver related causes include liver cirrhosis,
portal vein thrombosis, idiopathic portal fibrosis and
Budd-Chiari syndrome.
SAAG <1.1 g/dL means conditions associated with
normal portal pressure. This includes tuberculosis,
pancreatitis, serositis and peritoneal cancers
(peritoneal carcinomatosis).

Confusion Corner: Decrease in liver
transaminases
Intracellular enzymes leak from injured hepatocytes in active
or ongoing inflammation. So, progressive decrease in liver
transaminases should mean recovery from liver injury. However
this is not always necessary.
Decrease in liver transaminases could also mean that there are
very few hepatocytes left or functional reserve of liver is very
low. It must be interpreted in light of other liver tests.
For example if the synthetic function of liver is low
(Prothrombin Time is rising) and liver enzymes are decreasing, it
means that there are very few hepatocytes left and such
condition could rapidly progress to fulminant liver failure
(hepatic encephalopathy within 8 weeks of onset of acute liver
failure).
ALT is more specific and sensitive for liver damage than AST
(also found in skeletal muscles, heart, kidney, brain)
AST and ALT usually have similar increase. Notable exception
include alcoholic hepatitis in which AST/ALT is >2:1.

Drift may be visible after 10 seconds. The mechanism behind the
test is very simple. Pronators in the forearm are much powerful
than the supinators, an effect that would be exaggerated if the
person has upper motor neuron lesion.

Confusion Corner: Heparin and Warfarin
Therapy followed by Warfarin Therapy
Heparin binds to antithrombin III and enhances its activity
stabilizing the clot. Even more importantly it provides
anticoagulation until warfarin can begin anticoagulation fully.
Warfarin works by inhibiting formation of vitamin K dependent
factors (II, VII, IX, X). However first vitamin K dependent factors
to be affected are protein C and protein S, which are actually
anti-thrombogenic. Thus the action of warfarin could make it
initially thrombogenic.
For full anticoagulation, warfarin typically takes 5 to 7 days, up
to which heparin must be continued.
In DVT, LMWH should continue at least 2 days until INR in
target range (2-3). The therapy is usually for 6 weeks to 6
months. For patient with cancer or VTE or pregnancy, continue
6 months of LMWH without warfarin.

Is the solitary pulmonary nodule neoplastic?
A solitary pulmonary nodule is defined as a discrete, well-marginated, rounded
opacity less than or equal to 3 cm in diameter that is completely surrounded
by lung parenchyma, does not touch the hilum or mediastinum, and is not
associated with adenopathy, atelectasis, or pleural effusion.

Blood in Urine: Origin
Timing of Hematuria Location of lesion
Beginning of urination Urethra
End of urination (Terminal
hematuria)
Bladder or prostrate cause
(clots might be present in
bladder carcinoma)
Entire urination Ureter or kidney (no clots in
renal cause of hematuria)

Sick Sinus Syndrome
also known as tachycardia-bradycardia syndrome
secondary to tachycardia or bradycardia, atrial fibrillation or
thromboembolism may occur
may present with Stokes-Adams attacks, fainting, dizziness,
light headedness, chest pain, transient ischemic attack, stroke,
dyspnea, nausea, fatigue or palpitations
Very common indication for pacemaker placement
Atrial fibrillation if present needs to be treated:
Anticoagulation
Beta blockers
Cardioversion/Calcium channel blockers
Digoxin (in refractory cases)

Thrombolysis in Myocardial Infarction (TIMI)

What are the tests for H.pylori apart from non-
invasive Urea breath test?
Serology (antibodies to Helicobacter pylori but
remains positive even after infection is cleared)
Stool antigen test (detect H.pylori antigens in
stool, very sensitive and specific)
Endoscopic biopsy (gold standard but invasive,
can detect other issues like intestinal metaplasia,
mucosa associated lymphoid tissue or
widespread gastritis)

Clinical Pearls in Pancreatitis
Flank bruising (Grey Turner Sign)
Periumbilical discoloration (Cullen sign)
Discoloration over inguinal ligament (Fox’s sign)
Elevated serum lipase and amylase
Hypocalcaemia
Sentinel loop or Colon cut-off sign
Chain of lake appearance (chronic pancreatitis)

Management of Sickle Cell Disease in a Nutshell
Hydroxyurea stimulates production of fetal hemoglobin
thus preventing recurrent sickle cell crisis. Teratogenic
and can cause myelosupression.
Chronic transfusion therapy along with folic acid
supplementation to prevent macrocytosis secondary to
repeated RBC turnover
Antibiotics for febrile patients or patients with
leukocytosis (ceftriaxone, levofloxacin, moxifloxacin)
Prophylactic pneumococcal vaccination and antibiotics
for risk of infection by encapsulated bacteria
Cholecystectomy for recurrent cholelithiasis.

Mentzer Index
MCV (in fL)/RBC Count (in million/mm3)
Mentzer Index >13 suggests iron deficiency anemia (both number of
RBCs and size would decrease)
Mentzer Index <13 suggests thalassemia (RBC count is usually normal
but red cells are smaller and more fragile)
 Microcytic anemia causes:
 Thalassemia
 Anemia of chronic disease
 Sideroblastic anemia
 Iron deficiency anemia
 Lead poisoning (@TASIL)
Iron deficiency anemia is common. Failure to respond to iron
supplements indicate other etiologies as the likely cause of microcytic
anemia.

Crest syndrome is associated with anticentromere antibodies. Associated with
limited cutaneous scleroderma.

Amyotrophic Lateral Sclerosis in a Nutshell
Combined LMN and UMN deficits with no
sensory or oculomotor deficits
Fasciculations with eventual atrophy and
weakness of hands
Known as Lou Gehrig disease in US and motor
neuron disease in UK
Rilouzole treatment modestly increase survival
by decreasing presynaptic glutamate release

Rule of 17 for LMN lesions of cranial nerves:
Cranial Nerve (5 & 12): deviation towards same side, paralyzed side
Cranial Nerve (7 & 10): deviation towards opposite side, healthy side

UMN Facial Palsy LMN Facial Palsy
Lower face affected (inferior 1/4th part
contralateral to lesion), opposite to the
site of lesion. Upper face spared. The
reason is lower or ventral half of nucleus
receives only contralateral corticonuclear
fibers while upper or dorsal half of
nucleus receives fibers bilaterally.
Ipsilateral to lesion, whole upper and
lower face affected
Bell’s phenomenon doesn’t occur
(movement of eyeballs in upward and
outward direction when eyelids are
forcibly closed)
Bell’s phenomenon is seen. Weakening of
orbicularis oculi is noticed.
Facial muscles are not atrophied Fasciculation and muscle atrophy at
affected side
Corneal reflex preserved Corneal reflex lost
Usually with hemiplegia of same side Hemiplegia if present is usually crossed
(ipsilateral & contralateral presentation in
different body parts)
Site: Supranuclear Site: Nuclear & Infranuclear

Cerebellar Examination Points
Stance and gait
Heel-toe test
Romberg test
Heel-shin test
Finger nose test
Dysdiadochokinesis
Rebound phenomenon
Nystagmus
Reflex (pendular)
Tone (hypotonia)

What are four features to look in a
COPD Chest X-Ray?
Hyperinflated chest
Flattening of diaphragm
Narrow elongated
tubular heart
Crowding of ribs

Normal chest shape is B/L symmetrical and elliptical. AP to transverse
diameter is 5:7. Normal expansion of chest is 5-8 cm. Barrel chest has
equal AP and transverse diameter i.e. 1:1.
Both pigeon chest (forward protrusion of sternum & adjacent costal cartilages) &
funnel chest (exaggeration of normal hollowness on the lower end of sternum) could
occur in Marfan syndrome.

Respiratory
Percussion
Special Points
Anterior percussion Patient should sit erect with hands by his side.
 Clavicle: middle 1/3rd
 Supraclavicular region (Kronig’s isthmus): band of resonance 5-7
cm over supraclavicular fossa [Boundaries include scalene
muscles medially, acromion process laterally, clavicle anteriorly &
trapezius posteriorly]
 Infraclavicular region: 2nd to 6th ICS though cardiac dullness don’t
let note to be compared. Percuss preferably in contiguous
manner, not in zigzag manner.
Posterior percussion Patient should bend his head forward and keep his hands over the
shoulders to spread away the scapulas.
 Suprascapular (above spine of scapula)
 Interscapular
 Infrascapular up to 11th ICS
Lateral percussion Patient should sit with his hand held over his head
 Mid axillary line 4th to 8th ICS
The movement of plexor to strike the pleximeter is at the wrist joint. Sitting position is best for
percussion in respiratory examination as in supine and other positions there might be the alteration
of the percussion note by the underlying structures in which patient lies. The sites of auscultation
are also similar. Anteriorly, above clavicle to 6th rib, posteriorly above spine of scapula to 11th rib
and laterally to 8th rib.

• Parasternal heave is the
anterior movement of
the lower left
parasternal area
• Thrill are low frequency
vibrations in time with
cardiac cycle (just like
palpable equivalents of
murmurs)

AR
AS MS
MR
 Delayed upstroke (tardus)
 Crescendo decrescendo
murmur
 HOCM have same murmur
 Austin flint murmur probable
 High pulse pressure
 Water hammer/
Collapsing/Corrigan’s pulse
 Irregular pulse (Atrial
fibrillation)
 Loud S1
Early
diastolic
murmur
Mid
diastolic
murmur
Systolic
ejection click
murmur
Pansytolic/
Holosystolic
murmur
 Rheumatic fever: Mitral >
Aortic > Tricuspid > Pulmonary
 VSD, PDA & TR have same
murmur
 All right sided murmurs increases on inspiration & all left sided increases on expiration
 Left sided murmurs increases with increased preload (squat) & decreases on decreased preload (valsalva)
 Forward flow murmurs increase on decreased afterload (vasodilators) & backward flow murmurs increased on
increased afterload (handgrip)

Maximum score: 67
Mild alcohol withdrawal: ≤ 10
Moderate alcohol withdrawal: 11 to 15
Severe: ≥16

Normally the distance between xiphisternum to umbilicus and from umbilicus to
symphysis pubis is equal. Pregnancy or ovarian cyst displaces umbilicus upward.

Maddrey’s Discriminant function

Glasgow Alcoholic Hepatitis Score

Pleural effusion detection
• PA view: at least 200 mL
• Lateral decubitus view: at least 100 to 150 mL
• USG: at least 50 mL
Large volume aspiration (> 1.5 L) could lead to re-
expansion pulmonary edema.

What is the minimum amount of fluid in
ascites needed to elicit shifting dullness?
500 mL
Fluid thrill: 2L
Puddle sign (patient in knee wlbow position,
percuss from below): 120 mL
USG or CT scan: 100 mL
Diagnostic tap: 10-20 mL

Elevated hemidiaphragm (Hampton’s hump ) could also be seen in pulmonary embolism.

Rickety rosary (rachitic rosary) means bead like enlargement of the
costochondral junction.

Generalized lymphadenopathy is when 2 or more of the non contiguous lymph nodes
are affected.

What does aspirin changes in the
blood gas parameters?
• Respiratory alkalosis progressing to metabolic
acidosis
• Tinnitus is also seen. Treatment includes
alkalinizing the urine which increases the rate
of aspirin excretion.

Migraine criteria

Migraine Treatment in a Nutshell
Analgesics (PCM 1 gm, Aspirin)
Antiemetics (Metoclopramide 5-10 mg)
5HT1B agonists/Triptans (Sumitriptan,
Rizatriptan 50-100 mg PO)
If >5 attacks/month: Amitriptyline, Sodium
valproate, Propranolol

Causes of Clubbing

Reticulocyte index

10 steps of management of Medically
Unexplained Symptoms
1. Acknowledge distress
2. Elicit the patient's perspective
3. Focused examination
4. Specific reassurance
5. Discuss alternative explanations
6. Consider medications
7. General coping techniques
8. Specific stress solutions
9. Discuss responsibility
10. Appointment for review

Red flag signs of headache
• New and sudden onset of headache
• New development of headache after 50
• New headache with k/c/o malignancy/HIV/immune
system impairment
• Headache associated with focal neurological sign/CNS
disease including seizure
• Headache associated with signs of systemic illness
(fever/rash/stiff neck)
• Headache associated with papilledema
• Headache increasing in frequency and severity
• Headache following head trauma

Motivational interview components
1. Express empathy
2. Develop discrepancies
3. Avoid argumentation
4. Roll with resistance
5. Support self efficacy

Cannula Sizes
@ O Girl Why
Green? Then,
PBYP (like PPAP)

Coma Cocktail
• Dextrose
• Oxygen
• Naloxone
• Thiamine
(@DON’T)

CT Scan (Canadian Criteria)
1. Reduced level of consciousness following
head trauma
2. Sudden onset of reduced level of
consciousness with hemiplegia (CT
differentiates ischemic and haemorrhagic
CVA)
3. Gradual onset of reduced level of
consciousness with focal neurological signs
(space occupying lesion)

Dose of Paracetamol
• Therapeutic dose is 10-15 mg/kg
Toxic dose:
• More than 7.5 gm (around 15 tablets) – minimal
toxicity, severe liver toxicity if > 15 gm (30 tablets)
• In adults toxic dose is 150mg/kg
• In children under 12 years toxic dose is 200mg/kg

PCM Poisoning Stages

N-Acetylcysteine (NAC) for PCM Poisoning
• 150mg/kg in 200 ml 5% dextrose over 15 minutes
• Followed by 50mg/kg in 500 ml 5% dextrose over 4
hours
• Followed by 100mg/kg in 1000 ml 5% dextrose over
16 hours

No gastric lavage in:
• Acid/alkali (can cause damage as they come up)
• Kerosene (fumes causes chemical pneumonitis)
• Airway is not secure (GCS<8)
• Uncooperative patient

Sub-arachnoid haemorrhage Management
• Protecting the airway
• Managing blood pressure (Labetalol, Esmolol,
Nicardipine)
• Preventing rebleeding (bed rest, stool softeners,
mild sedation, hydration)
• Preventing and treating raised ICP (Mannitol 25-100
gm qid)
• Managing vasospasm (Nimodipine 60 mg 4 hourly)
• Managing seizure activity (Phenytoin prophylaxis)
• Preventing pulmonary embolism

Raised ICP Management
• Position head up (30-45 degrees)- facilitate venous
drainage
• Avoid activities that increase ICP (suctioning, gagging
or straining)
• Treat hyperthermia
• Anticonvulsant therapy for seizures
• Use of diuretics (mannitol, urea and glycerol)
• Fluid restriction (can give dextrose if hypoglycaemic)
• Avoid compression of jugular veins or kinking of neck

Organophosphate management
Atropine:
0.6-2mg IV, repeated every 3-5 mins until secretions
controlled, skin is dry and there is sinus tachycardia
(atropinization)
Oximes:
30 mg/kg bolus followed by 8 mg/kg/hr

Special features of seizure Vs syncope
Seizure:
• Aura (e.g. olfactory)
• Tongue biting
• Post-ictal confusion and amnesia
• Cyanosis (@ATP Cyanosis)
Syncope:
• Rapid recovery
• Clear precipitating event (e.g. pain, stress, straining
during micturition or defaecation)
• Feeling of light headedness before faint
• Gradual loss of consciousness

Types of Stress Tests Positive Features (Need for
Cardiac Catheterization)
Exercise ECG  Sensitive if normal resting ECG and
patients are able to raise heart rate
close to (220-Age).
 Positive tests include ST segment
depression, chest pain, hypotension,
onset of heart failure or arrhythmias.
Exercise or dobutamine
echocardiogram, dipyridamole
perfusion study. Isotopes like
Thallium-201 and Technetium-
99m.
Wall motion abnormalities (akinesis or
dyskinesis). Decreased uptake of isotope
from blood in ischemic areas of
myocardium.

To elicit Homan’s sign, firstly thigh is supported with one hand
and then knee is flexed. After that ankle is abruptly dorsiflexed
to detect whether deep calf pain develops.

A-a gradient implies difference in oxygenation status between alveoli and
arterial blood. Increased A-a gradient is seen in pulmonary embolism,
pulmonary edema and right to left vascular shunts.

Somogyi effect is basically bodily response as rebounding high glucose
level in a response to low blood glucose with the aid of counteracting
hormones viz. glucagon, adrenaline, cortisol.

Marcus Gunn Pupil in Swinging
Flashlight Test
Argyll Robertson pupil are miotic, irregular in shape which accommodate (near
reflex intact) but don’t react (light reflex very slow or absent). Classical finding
in neurosyphilis.

Biliary colic is a misnomer as this is not a pain that comes and goes. It may fluctuate over time in
intensity, but it does not disappear. It is constant. It comes on rather suddenly, either starting as an
intense pain or building up in intensity quickly to reach a peak. It remains constant (though possibly
fluctuating in intensity) and then disappears, usually gradually. The duration of the pain is 15
minutes to several hours. If the pain is shorter than 15 minutes, it is unlikely to be caused
by gallstones. If the pain lasts longer than several hours it is either not biliary colic, or the gallstone
causing the biliary colic has led to a complication like acute cholecystitis.

What do you understand by Becks triad?

Life Threatening Causes of Chest Pain
I. Acute Coronary Syndrome
II. Cardiac tamponade
III. Aortic dissection
IV.Pulmonary embolism
V. Tension pneumothorax
VI.Mediastinits
Levine’s sign(clenched fist over chest to describe squeezing or
crushing pain) is typically used by patients with ischemic chest pain.
Never miss gastrointestinal pain or musculoskeletal pain (fractured
ribs, trauma or costochondritis) in your differentials.

ECG Evolution in non-reperfused MI
1. Peaked T waves (minutes)
2. ST segment elevation & progression (minutes
to hours)
3. Loss of R wave, Q wave formation (hours to
days)
4. T wave inversion (days)
5. T wave normalization, persisting Q wave
(weeks to months)

Time for Reperfusion Therapy

Rheumatoid Arthritis New Criteria

Classical Rheumatoid Arthritis Criteria

Stress Induced Cardiomyopathy

Remember, Jod-Basedow effect is hyperthyroidism following
administration of iodine or iodide, either as a dietary supplement or as
iodinated contrast for medical imaging.

Secondary Hypertension Clinical Pearls

Normal Pressure Hydrocephalus (3Ws)
1. Wet: Urinary incontinence
2. Weird: Dementia
3. Wobbly: Wide based gait/Ataxia

Spleen Percussion Techniques for
Splenomegaly:

Characters of JVP to differentiate
from Carotid pulse or Radial pulse
• JVP is:
Multiphasic (beats twice per cardiac cycle)
Non palpable
Occludable
Varies with Head Up Tilt (HUT) and inspiration
(Kussmaul sign: paradoxical rise JVP on inspiration)
Abdominojugular reflex (press RUQ: rise JVP)

JVP Waveform in a Nutshell
• a: right atrial contraction
• c: right ventricular contraction (tricuspid bulging towards
right atrium)
• x: descent of tricuspid towards right ventricle on ventricular
systole
• v: Atrial filling (@Filling=Villing)
• y: Emptying of right atrium with opening of tricuspid valve
(@EmptYing of RA)

JVP level
• Maximum 4cm from
sternal angle: 9cm
from right atrium
• 4cm of water
• 1 mm of Hg = 1.36
mm of H20

BUN Vs Urea

 <10 mOsm/kg (Measured serum osmolality - Calculated serum osmolality) is
normal osmol gap.
 Add Ethanol/3.7 (ethanol is not an ideal osmole in solution so divided by 3.7
instead of 4.6) in case of alcohol consumption.

Respiratory failure I and II

Central Vs Peripheral Vertigo
Central Peripheral
Sudden onset of weakness or sensory loss
in one half of the body
Recurrence of vertigo lasting less than a
minute (BPPV)
Impairment of gait and posture Ear symptoms
Associated with headache or other
migrainous phenomenon
Drugs like aminoglycosides, cisplatin,
phenytoin, benzodiazepines
Risk factors: HTN, DM, smoking or
vascular disease
Nausea, vomiting, ataxia and nystagmus
(cerebellar lesion)
Brainstem lesion features like diplopia,
visual loss, dysphagia, dysarthria,
weakness, ataxia, etc.
Similar drugs causing cerebellar toxicity

Keith-Wagener-Barker classification
of Hypertensive Retinopathy
• I: Thickening of arterioles, tortuosity and
increased reflectiveness (silver wiring)
• II: Grade I with Focal arteriolar constriction
(spasms). AV nicking (arteriole crossing a venule compressing
the vein)
• III: Grade II with Haemorrhages (flame
shaped), cotton wool exudates (ischemia) and
hard waxy exudates (lipid deposition)
• IV: Grade III & Papilledema

Points to ensure that you’re palpating
spleen and not kidney
• Spleen is not ballotable
• Spleen has no palpable upper border (the ribs
overlie its top)
• Spleen descends towards RIF on inspiration
• Direction of enlargement of spleen is towards
RIF (kidney towards lumbar region)
• Spleen is dull to percussion (kidney resonant,
colon being anterior)
• Splenic notch may be felt

Normal direction of flow of blood in the veins over the
abdomen is -
Above the umbilicus - Upwards
Below the umbilicus - Downwards
IVC obstruction
Above the umbilicus - Upwards and away from the
umbilicus.
Below the umbilicus - Towards the umbilicus.
SVC obstruction — From above downwards
In a prominent vein, after emptying the vein release one index finger
distal to heart: if it fills up then flow is towards the heart. Vein
remains empty, flow is away from the heart.

Osteoarthritis
Osteoarthritis usually spares MCP joint while RA typically involves
MCP, PIP joints and spares DIP joints.

Lupus anticoagulant is actually a misnomer. In vivo, it acts as a prothrombotic agent. The
name “lupus anticoagulant” derives from their properties in vitro, as these antibodies
increase laboratory coagulation tests such as the aPTT probably due interference with
phospholipids used to induce in vitro coagulation.

K is a constant with a value of 0.413 for children.

Diabetes Complications Classification
Macrovascular Microvascular Peripheral
neuropathy
Stroke Retinopathy
Coronary Artery Disease Nephropathy
Peripheral vascular
disease (Foot gangrene)

Diabetes Ketoacidosis Criteria
1. Hyperglycemia (≥ 200 mg/dL)
2. Hyperketonemia (≥ 3mmol/L and Ketouria 2+
on dipstick)
3. Metabolic acidosis (HCO3 < 15 mmol/L
or/and pH<7.3)

DKA Management in a Nutshell
IV fluids: 2-3 L of 0.9% saline in 1-3 hours
Then, 0.45% NS at 250-500 mL/hr
When glucose reaches 200 mg/dL, add dextrose
5% with 0.45% NS at 150-200 mL/hr
Insulin 0.1 units/kg. If no response in 2-4
hours, increase two to three fold.
Always monitor potassium level with insulin. If
<3.3 mEq/L, correct it. If >5.2 mEq/L, no
further supplements.

Indications of Dialysis in ARF

What are five causes for anemia in chronic
alcoholics and patient with chronic renal failure?
Chronic alcoholics Chronic renal failure
Chronic GI tract blood loss Decreased erythropoietin
Nutritional deficiencies Decreased erythropoiesis secondary to
toxic effect of uremia to marrow
precursor cells
Hypersplenism Decreased RBC survival
Direct suppressive action on bone
marrow
Increased blood loss due to capillary
fragility and poor platelet function
Zieve’s syndrome on withdrawal Decreased dietary intake and reduced
iron absorption
Hemodilution

Confusion Corner: Trousseau Sign
Trousseau sign of latent tetany: blood pressure cuff
inflated over 20 mm Hg of systolic pressure to occlude
brachial artery for 3 to 5 minutes when carpopedal spasm
with flexion at wrist and MCP joint, extension at IP joint
and adduction of fingers occurs
Trousseau sign of malignancy: Migratory thrombophlebitis
Troisier sign: left supraclavicular node enlargement
(Virchow’s node)
Never confuse concept of eliciting trousseau sign with tourniquet test for detecting
hemorrhagic tendency in dengue (blood pressure cuff inflated for 5 minutes at midpoint
pressure between systolic and diastolic pressures to see if >10 to 20 petechiae per square
inch are present). Here cuff is inflated 20 mm Hg above systolic not in between.

Dermatomyositis

Domiciliary oxygen (at least 15 hours a day) in patient with heart
failure or elevated hematocrit: PaO2<60 mmHg & SpO2<90%

Approach to Neuropathic Disorders:
7 Key Questions
1. What systems are involved?
 Motor, sensory, autonomic, or combinations
2. What is the distribution of weakness?
 Only distal versus proximal and distal
 Focal/asymmetric versus symmetric
3. What is the nature of the sensory involvement?
 Temperature loss or burning or stabbing pain (e.g., small fiber)
 Vibratory or proprioceptive loss (e.g., large fiber)
4. Is there evidence of upper motor neuron involvement?
 Without sensory loss
 With sensory loss

5. What is the temporal evolution?
– Acute (days to 4 weeks)
– Subacute (4 to 8 weeks)
– Chronic (>8 weeks)
6. Is there evidence for a hereditary neuropathy?
– Family history of neuropathy
7. Are there any associated medical conditions?
– Cancer, diabetes mellitus, connective tissue disease or
other autoimmune diseases, infection (e.g., HIV, Lyme
disease, leprosy)
– Medications including over-the-counter drugs that may
cause a toxic neuropathy
– Preceding events, drugs, toxins

Asbury criteria for GBS includes cytoalbumin dissociation meaning that CSF
shows increase in protein content without corresponding rise in WBCs.

HAS-BLED points 3+ means very high risk of bleeding.

In VT though there is presence of AV dissociation, occasionally a P wave is conducted to the
ventricles producing normal sinus beat in the middle of tachycardia (capture beat). When
conducted beat fuses with impulse from tachycardia, it’s k/a the fusion beat.

Treatment (Mobitz II and 3rd degree block) is usually atropine & cardiac
pacing.

Antiretroviral Regimens
HAART regimen (WHO): Recommended first-line regimen
2 nucleoside reverse transcriptase inhibitors (NRTIs) +1 non-
nucleoside reverse transcriptase inhibitor (NNRTI):
ZDV + 3TC + NVP (Zidovudine + Lamivudine + Nevirapine)
ZDV + 3TC + EFV (Zidovudine + lamivudine + Efavirenz)
d4T + 3TC + NVP / EFV (Stavudine + Lamivudine +
Nevirapin/Efavirenz)
Alternative regimen:
Triple NRTIs
2NRTI + PI

Nepal Guidelines for ART
CD4 count < 500/mm3 regardless of WHO staging
All patient of HIV regardless of WHO staging or
CD4 count if:
 Co infected with active TB disease
 Co infected with HBV with evidence of severe CLD

Management of CNS infection in HIV
Cryptococcus Infection Toxoplasmosis Infection
Induction (for 2 weeks):
IV liposomal amphotericin B 4-6 mg/kg
daily plus
5-flucytosine 25 mg/kg QID
Maintenance:
Fluconazole 400 mg/day PO for 8
weeks
And then, fluconazole 200 mg/day
until CD4+ T cell count has increased to
>200 cells/ mm3 for 6 months in
response to HAART
Raised ICP: to maintain CSF pressure
<20 cm H2O
-Repeated therapeutic Lumbar
puncture
Sulphadiazine or clindamycin with
pyrimethamine and folinic acid for 6 weeks
with Dexamethasone if mass effect.
Cotrimoxazole is also equally effective.
Stop therapy when CD4 >200 cells/mm3 for
3 months on suppressive HAART

Splenectomy predisposes to encapsulated organisms infection because though
microorganisms are coated with IgG and C3b ready for the process of opsonization,
phagocytosis does not occur. Encapsulated organisms causing risk of infection are similar to
complement deficiency.

Acknowledgements:
Best of the best slides, pictures and information on
the web. Special thanks to all those brilliant minds
for their act of creation and compilation of
scientific material without which this work would
not be possible
• Davidson’s Principle and Practice of medicine
• Harrison’s Principles of Internal Medicine
• Kumar and Clark Clinical Medicine
• Lecture Notes
• Bedside Clinics in Medicine, Kundu
• Pearls in Medicine for Students, Kundu
Dr. Aryan (Anish Dh

Why do almost all toppers lie about
their study schedule?
https://medium.com/@anishdhakal718/why-do-
topper-lie-about-their-study-schedule-c8f6e679c97d

Medicine Review Booklet by Dr. Aryan (Medical Booklet Series by Dr. Aryan Part 19)

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