In this presentation I have tried to cover renal disorder associated with vascular pathology of kidney. Classification, various disorder in detail with histopathology images H&E and special stains and clinical presentations. Hope it helps understanding the entity better.
Brief explanation of each *refer harrison textbook for details causes of TIN
Acute interstitial nephritis
Chronic interstitial nephritis
Reflux nephropathy
Papillary necrosis
Sickle-cell nephropathy
In this presentation I have tried to cover renal disorder associated with vascular pathology of kidney. Classification, various disorder in detail with histopathology images H&E and special stains and clinical presentations. Hope it helps understanding the entity better.
Brief explanation of each *refer harrison textbook for details causes of TIN
Acute interstitial nephritis
Chronic interstitial nephritis
Reflux nephropathy
Papillary necrosis
Sickle-cell nephropathy
This presentation comprises of congenital anomalies of kidney and urinary tract made concise and in depth for PG preparation. It contains all important topics of the regarding subject covered in detail.
A simple description of a less understood topic in Intensive Care Medicine. Aim to make understanding and management easy for the residents and prevention steps for all ICU workers.
Pyelonephritis
It is the inflammation of the kidney & upper urinary tract that usually results from the bacterial infection of the bladder.
Pyelonephritis can be classified in several different catagories:
-acute pyelonephritis
-chronic pyelonephritis
-xanthogranulomatous pyelonephritis
This presentation comprises of congenital anomalies of kidney and urinary tract made concise and in depth for PG preparation. It contains all important topics of the regarding subject covered in detail.
A simple description of a less understood topic in Intensive Care Medicine. Aim to make understanding and management easy for the residents and prevention steps for all ICU workers.
Pyelonephritis
It is the inflammation of the kidney & upper urinary tract that usually results from the bacterial infection of the bladder.
Pyelonephritis can be classified in several different catagories:
-acute pyelonephritis
-chronic pyelonephritis
-xanthogranulomatous pyelonephritis
Renal artery stenosis is the leading cause of secondary hypertension and may lead to :
Resistant (refractory) hypertension,
Progressive decline in renal function, and
Cardiac destabilization syndromes (Flash pulmonary edema, recurrent heart failure, or acute coronary syndromes)
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
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Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
2. Introduction To Renovascular Disease
(RVD)
The Kidneys depend on systemic blood pressure
(SBP) to maintain adequate RBF and hence
adequate GFR, tubular function and overall salt
and water balance
This explains the vulnerability of kidneys to
diseases involving the renal vasculature
Vascular injury to kidneys is usually a
manifestation of generalized vascular pathology
3. Classification of RVD according to
anatomic location of vasculopathy
Renal Arteries Renal Arterioles and
microvasculature
Renal Veins
Thromboembolic
occlusion
Atheroembolic Disease
(cholesterol embolism
syndrome CES)
Renal Vein
Thrombosis (RVT)
Renal Artery Stenosis
(RAS), and
Ischemic renal
disease
Hypertensive arteriolar
Nephrosclerosis
Thrombotic
Microangiopathies:
1. Hemolytic Uremic
Syndrome (HUS)
2. Thrombotic
Thrombocytopenic
Purpura (TTP)
Scleroderma
Sickle cell nephropathy
4. Thromboembolic Occlusion of Renal
Arteries
Causes:
►►Intrinsic pathology in renal vessels:{In situ
thrombosis}
Post-traumatic.. Young patients (blunt trauma, deceleration injury,..)
Atherosclerotic.. Old patients
Dissection/Aneurysm/Arteriography
Inflammatory: Takayasau, syphilis, systemic vasculitis,
thrombangitis obliterans
►► Embolization: {originating in distant vessels};
much more common (90%) and usually unilateral
Tumor/Fat emboli
Emboli from left heart (most common), as left mural thrombus
following MI or AF, or bacterial endocarditis, septic/aseptic
valvular vegetations..
►► Paradoxical emboli, passing through patent foramen
ovale or ASD
5. Clinical Manifestations Of
Thromboembolism
Difficult to diagnose, require high index of
suspicion
Variable, depend on: extent/time course of occlusion
and state of pre-existing renal circulation
Acute renal thrombosis/infarction ---------->
o Sudden onset of flank pain/tenderness (? absent in
55 %)
o Fever/nausea/vomiting
o Hematuria (microscopic)
o Deteriorated renal function: transient (unilateral), or
severe (bilateral)
o Hypertension, usually transient (renin release in peri-
infarction zone)
o Elevated TLC, AST, LDH, ALP (renal enzymes in
infarction)
6. Clinical Manifestations Of
Thromboembolism
Gradual unilateral occlusion --> may go
undetected
Patients with RAS & established collateral
circulation have no symptoms (little/no
infarction)
----------------------
** Thus, the spectrum of clinical manifestations lies
between some extremes in different occasions:
ARF
Unexplained Progressive Azotemia (old patient ±
refractory HTN)
HTN + Azotemia (renal transplant)
7. Diagnosis and Treatment Of
Thromboembolism
Diagnosis:
MRA
Spiral CT
Duplex U/S
Renal Arteriography
Renal Scintigraphy
± Echocardiography
TTT:
Surgical revascularization (for traumatic renal A. thrombosis),
mortality rate:11-25%
Intra-arterial thrombolytic (for iatrogenic occlusion of renal As,
as a result of angiography or angioplasty)
Adequate hydration/HTN Control
Anticoagulation
Renal replacement therapy (RRT)
N.B. The warm ischemia time beyond which recovery of renal
function would not be anticipated, is several hours..!!
8. Renal Artery Stenosis (RAS) and
Ischemic Renal Disease
RAS Ischemic Renal
Disease
Prevalence:
2-4 % in general population
30-40 % in accelerated HTN
and renal insufficiency
Causes:
Atherosclerosis:(ARV
D)
o90 %
oElderly
Fibromuscular
Dysplasia:
o5-10 %
oYoung
Atherosclerosis of 1 or both renal
As
Elderly male
± HTN
Often with atherosclerotic PVD
(68%)
IHD (45%)
CHF (33%)
History of stroke (28%)
Progressive loss of renal function
9. Atherosclerotic Renovascular
disease(ARVD)
It accounts for >90% of all RVD, in patients > 55, or < 30
Ys of age
Lesions of RAS are 90% ostial (within the1st one cm of
renal artery origin)
It can be demonstrated in:
o >10% of patients undergoing coronary angiography
o >40% with peripheral vascular disease (PVD), with > 5 vessels
involvement
o 30% with congestive cardiac failure (CCF), aged >70 years
o 15-20 % with ESRD
It is increased with aging and is associated with common
atherogenic risk factors:
o Hypertension
o Hypercholesterolemia
o Smoking
o Diabetes
10. Clinical Presentations of ARVD
Hypertension (HTN), with Chronic Kidney Disease (CKD),
a pro-atherogenic state make the incidental finding of
ARVD, rather than being the cause of it..?
Epigastric bruit
Hypokalemia and metabolic alkalosis
Flash pulmonary edema(5%):
o Sudden onset of acute heart failure in absence of myocardial
ischemic event
o Commonly at night(due to posture-related redistribution of fluid
or may be due to diurnal variations of vasoactive peptides)
o Mechanism may be due to reduced natriuretic ability, coupled
with LVH and severe HTN in patients with severe bilateral
RAS
Acute Kidney Injury (AKI), due to arterial occlusion
Ischemic ATN, or related to ACE-I (after 1-14 days)
11. Prognosis of ARVD
Renal outcome is determined by the presence of
parenchymal disease giving the picture of
ischemic nephropathy (intrarenal atheroma, or
cholesterol embolization)
The correlation between the severity of proximal
lesions(degree of stenosis or occlusion) and renal
function is poor.. (?? Variable outcome for
revascularization)
Poor prognosis (5-year survival<20 %)
12. Fibromuscular Dysplasia (FMD)
It accounts for 10% of all RVD
Most commonly in young women (20-35 Ys)
The stenotic lesions are distal and appear like
“string of beads”, at angiography
Clinically, presented with severe HTN, but renal
failure is unusual
It is usually associated with other arterial
lesions (carotid stenosis in 10% of cases)
Revascularization cure the HTN and restores
the kidney function completely; because the
kidney beyond the FMD, is usually healthy
13. Radiological Diagnosis of RAS
MRA:
o Optimum, non-invasive
o 3-D phase contrast
o Safe in CKD stages 3 and 4
Gadolinium-based MRI: ? Fear of related Nephrogenic systemic
fibrosis (NSF)
Duplex /Color Doppler U/S:
o Disparate kidney size (> 1.5 cm in bipolar length)
o Can be combined with measurement of proximal renal blood flow velocity,
with intrarenal resistive index
o Accurate for detection of ARVD and for assessment of severity of RAS
o Time-consuming/Highly operator-dependent
Captopril renal Scintigraphy: if unilateral disease and S. creat
< 2 mg/dl
CT-angiography, can be complicated by radiocontrast
nephropathy
Conventional intra-arterial arteriography:
o Reserved for patients with complex anatomy
o For confirmation of RAS prior to revascularization
14. Treatment of RAS
Conservative medical management:
• Cessation of smoking/weight loss/exercise
• Strict Control of HTN
• Lipid lowering agents
• Aspirin
Revascularization, especially successful in significant RAS
associated AKI, or with flash pulmonary edema:
o Percutaneous Transluminal Renal Angioplasty (PTRA), with
stenting (PTRAS), in >95% of cases
o Surgical reconstruction: celiac, or mesenteric –to- Renal
Bypass, in remainder of cases
Balloon angioplasty:
o Uncontrolled HTN
o FMD (less effective in ARVD, recoil after dilatation can occur because
of the rigid lesions or because of dissection)
o Success rate:82-100 %
o Recurrence rate: 10 % (follow-up with duplex U/S)
15. Atheroembolic RVD
Cholesterol embolisation syndrome (CES) is occurring in:
I. Elderly patients with widespread atherosclerosis (almost
exclusively)
II. As complication of abdominal aorta/renal artery manipulation or
surgery
III. As a consequence of angiography or PTRA
Clinically:
I. Renal insufficiency &/or HTN
II. Livideo reticularis
III. Evidence of embolisation in other organs: Cerebrovascular
events, retinal artery occlusion, acute pancreatitis, ischemic
bowels, gangrene of extremities
Urine analysis:
I. Cholesterol crystals (not usually present)
II. Increased cellularity
III. Proteinuria (mild)
IV. Eosinophiluria
Eosinophilia: 11-16 %
16. Treatment of CES
Control HTH (avoid hypotension)
Adequate hydration
? Anticoagulants may delay healing of ulcerated
atherosclerotic lesions
Dialysis may be needed
17. Hypertensive Nephrosclerosis
Due to unopposed or sustained ↑ in intraglomerular
capillary hydrostatic pressure
Great risk in African-Americans, elderly and those
with high SBP
Pathogenesis:
o Stimulation of Renin release due to activation of
RAAS
o Reduced natriuretic capacity, due to CKD
o Disorganization of intrarenal vasculature: vascular
wall thickening and luminal obliteration
o Widespread interstitial fibrosis and
glomerulosclerosis
18. Hypertensive Nephrosclerosis
►► Benign nephrosclerosis:
HTN > 10-15 Ys
Kidneys become a victim of adverse effects --->Pronounced
medial vascular injury and progression to ESRD (2-5 %)
Reduced kidneys size on U/S
Unremarkable urinary sediment; except for proteinuria < 1.5
gm/day (? Asymptomatic)
Time of initiation of effective ttt with ACE-Is/ARBs, together with
patient compliance and careful follow-up are important
Target BP control is:
<130/80, in patients with CKD
<125/75, in patients with significant proteinuria
19. Hypertensive Nephrosclerosis
►► Malignant (accelerated) HTN:
Abrupt ↑ of DBP > 130 mmHg renal ischemia and renin production
Intimal injury Severe tubular and glomerular ischemia ARF
Headaches, seizures/? Stroke, encephalopathy..
Grade 3 or 4 retinopathy, with hemorrhages, exudates,
papilledema
? Microangiopathic hemolytic anemia
↑ of serum urea and creatinine
Enlarged kidneys on U/S
? Active urinary sediment: Proteinuria (nephrotic range) and
hematuria (gross, or microscopic): AKI
Emergency situation needing agressive BP control can reverse
renal functions: Parentral Na nitroprusside.. Smooth control over
36-48 Hs
20. Thrombotic Microangiopathies
I. Hemolytic Uremic Syndrome (HUS)
II. Thrombotic Thrombocytopenic Purpura
(TTP)
In both conditions, there is:
Microangiopathic hemolytic Anemia (MAHA), with
anemia, RBCs fragmentation, schistocytes,
intravascular PLT clumping and hence
thrombocytopenia
Typical renal histological lesions include
intraglomerular platelet and fibrin thrombi, with
ischemia and arteriolar lesions
21. Hemolytic Uremic Syndrome
(HUS)
Commonest cause of AKI in children
Children (< 4 years) ------> 90 % of cases
Adults ---------> 5 cases/million/ Year
22. Forms of HUS
1- Typical, or Diarrhea-associated (D+ HUS):
o Onset is explosive, with AKI
o Verotoxin-producing E.Coli O157:H7 (VTEC), with damage to the
vascular endothelium(largely confined to kidneys)
o ? Associted Shigella dysentriae
o 90% ----->Good recovery
o 40% ----->Decreased GFR (long term follow-up)
o 5% ------>Mortality during acute illness
o Disease monitoring by: PLT count and RBCs fragmentation
2- Atypical, or (D-HUS):
o Older children and adults, most of them have no diarrhea
o ? Familial, associated with factor H deficiency which limit cleavage of
unusual large von Willebrand; leading to continuing platelet activation
o Poorer prognosis, death in > 50 % of cases
23. Treatment of HUS
Mainstay of therapy:
1. Fresh Frozen plasma (FFP) infusion
2. Plasma exchange
They are more effective in adult D+ HUS than in
childhood forms; in atypical D- form, they lower
the risk of ESRD and mortality
24. Thrombotic Thrombocytopenic Purpura
(TTP)
Explosive AKI is less prominent
Neurological abnormalities are usual
Two main Forms:
Acute TTP Relapsing TTP
90 % Adults are usually affected,
with a chronic form of the
disease
Abrupt onset of fever,
neurological signs and purpura
Clinical condition similar to
atypical form of HU$
Survival now approaches 90 % ? Familial HU$ / TTP
Treatment: FFP infusion and plasma exchange
25. 2ry Causes of HUS and TTP
Pregnancy-Associated Thrombotic
Microangiopathy:
TTP
HELLP
Post-partum HUS
HIV - Associated Thrombotic Microangiopathy
Cancer - Associated Thrombotic Microangiopathy
Drugs: ex: Ciclosporin
26. Systemic Sclerosis
Renal involvement (50 %), in longstanding disease >
20 Ys..
Mild proteinuria is usually present ± HTN
Sclerodermal renal crisis, in 10-25 % of type 3
scleroderma:
o Accelerated HTN
o Microangiopathic hemolytic anemia
o AKI
Pathology:
o Intimal proliferation of interlobular arteries, with deposition of
mucoplysaccharides: Onion-Skin appearance
o Fibrinoid necrosis of afferent arterioles 2ry Glomerular
ischemia
Treatment: RAA-blockade, ± Non-DHPs, ±
Vasodilators (minoxidil) for HTN control.. Renal
function can recover
Poor prognosis; because of other organ
involvement, especially restrictive cardiomyopathy
27. Sickle Cell Nephropathy
Hypoxic/hypertonic medulla Sickling Recurrent
papillary infarction Papillary necrosis:
o Often Silent
o ? Repeated UTI (chronic renal insufficiency)
o Hematuria (50 %)
Vasa Recta Obliteration Compromisation of
medullary counter-current system ↓Urinary
concentrating ability Volume depletion
Nephrotic syndrome (4 %)
Distal RTA (type 4) ↑ K+ / ↑ Cl- metabolic
acidosis
MPGN FSGS
28. Treatment of sickle cell nephropathy
Avoid:
K+ supplements/K+ sparing diuretics
NSAIDs
TTT of volume depletion:
Isotonic/hypotonic solutions (according to serum Na values)
TTT of hyperkalemia:
K+ exchange resins (Na polystyrene or kayexalate, oral or per
rectum)
Shohl’s solution
Na HCO3 tablets
Loop diuretics
TTT of hematuria:
ɛ aminocaproic acid: in life threatening conditions, ? Fear of
thrombosis/uretral obstruction
Mannitol/ Loop Diuretics: (reduce medullary tonicity)
Na HCO3: (reduce medullary tonicity)
29. Renal Vein Thrombosis (RVT)
Causes of RVT
Nephrotic Syndrome:
(Loss of antithrombin III in urine/Protein C & S deficiency)
Renal Cell Carcinoma:
(Invasion of renal vein)
Volume Depletion:
(Impaired RBF)
Pregnancy/Estrogen therapy:
Extrinsic Compression:
{L.Ns, tumors, aortic aneurysm, retroperitoneal fibrosis or abscess,..}
(Sluggish renal venous flow)
Others:
{Sickle cell nephropathy, amyloidosis, diabetes, vasculitis, allograft
rejection}
30. Clinical Manifestations of RVT
Depend on extent and rapidity of occlusion:
1. Acute:
o Nausea/vomiting
o Flank Pain
o Hematuria
o Leucocytosis
o Compromised renal functions
o Increased renal size on U/S
2. Chronic:
o Dramatic ↑ of proteinuria
o Tubular Dysfunction: Glucosuria, aminoaciduria, phosphaturia
and impaired urinary acidification
31. Diagnosis of RVT
Investigations:
o MRV
o Doppler U/S: Not sensitive in “segmental” thrombosis
o Selective renal venography
o IVP: Calyceal stretch and ureteric notching
TTT:
o Heparin, for 7-10 Ds
o Warfarin, for one year (or indefinitely)
o Fibrinolytics, for acute RVT associated with ARF
33. Question 1
A 38-Y-old woman was brought to the ED because
of headache, difficulty in concentration and
slurred speech. She had previously been in
excellent health. She was found to have fever,
anemia (Hb=8.4 gm/dl) and profound
thrombocytopenia (PLT=30.000). Peripheral blood
smear shows schistocytes. S. LDH was 5 times
above the normal limits. The most likely diagnosis
is:
A. ITP
B. Thalassemia major
C. TTP
D. Autoimmune hemolytic anemia
E. Aplastic anemia
34. Answer 1
A 38-Y-old woman was brought to the ED because
of headache, difficulty in concentration and
slurred speech. She had previously been in
excellent health. She was found to have fever,
anemia (Hb=8.4 gm/dl) and profound
thrombocytopenia (PLT=30.000). Peripheral blood
smear shows schistocytes. Serum LDH was 5
times above the normal limits. The most likely
diagnosis is:
A. ITP
B. Thalassemia major
C. Thrombotic Thrombocytopenic Purpura
(TTP)
D. Autoimmune hemolytic anemia
35. Question 2
A two-year-old boy with sever diarrhea, presents to the ED
with oliguria, fever, chills and pain in the flanks.
Examination revealed severe dehydration, lumbar
tenderness and the right kidney was palpable and tender.
BP was 100/40. Urine examination revealed hematuria and
proteinuria. Serum urea and creatinine were raised and
serum albumin was normal. CBC and peripheral smear
appear normal. The most probable diagnosis is:
A. Post-streptococcal GN
B. Nephrotic $
C. Hemolytic Uremic Syndrome (HU$)
D. Renal vein thrombosis (RVT)
E. Septic shock
36. Answer 2
A two-year-old boy with sever diarrhea, presents to the ED
with oliguria, fever, chills and pain in the flanks.
Examination revealed severe dehydration, lumbar
tenderness and the right kidney was palpable and tender.
BP was 100/40. Urine examination revealed hematuria and
proteinuria. Serum urea and creatinine were raised and
serum albumin was normal. CBC and peripheral smear
appear normal. The most probable diagnosis is:
A. Post-streptococcal GN
B. Nephrotic $
C. Hemolytic Uremic Syndrome (HU$)
D. Renal vein thrombosis (RVT)
E. Septic shock
37. Question 3
A 23-Y-old woman presents with marked swelling of the ankles
following a mild URT infection. Dipstick urine analysis
demonstrates: protein +++, with no hematuria.
Plasma creatinine was 68 mmol/l. Albumin 2.3 gm/dl.
Cholesterol 8.9 mmol/l (=360 mg/dl). Urinary protein
excretion 12 gm/24 Hs.
Renal biopsy was performed and shows minimal change
glomerulopathy. The patient was commenced on
prednisolone 60 mg/d and simvastatin.
Seven Days later, urine protein +++ and blood ++. She has
some loin pain and plasma creat was 106 mmol/l.
What is the most likely complication that had occurred?
A. Renal vein thrombosis
B. Interstitial nephritis 2ry to simvastatin
C. Obstruction 2ry to a sloughed papilla
D. Peri-nephric hemorrhage 2ry to renal biopsy
E. Acute crescentic change of minimal change nephropathy
38. Answer 3
A 23-Y-old woman presents with marked swelling of the ankles
following a mild URT infection. Dipstick urine analysis
demonstrates: protein +++, with no hematuria.
Plasma creatinine was 68 mmol/l. Albumin 2.3 gm/dl.
Cholesterol 8.9 mmol/l (=360 mg/dl). Urinary protein
excretion 12 gm/24 Hs.
Renal biopsy was performed and shows minimal change
glomerulopathy. The patient was commenced on
prednisolone 60 mg/d and simvastatin.
Seven Days later, urine protein +++ and blood ++. She has
some loin pain and plasma creat was 106 mmol/l.
What is the most likely complication that had occurred?
A. Renal vein thrombosis
B. Interstitial nephritis 2ry to simvastatin
C. Obstruction 2ry to a sloughed papilla
D. Peri-nephric hemorrhage 2ry to renal biopsy
E. Acute crescentic change of minimal change nephropathy
39. Question 4
A 33-Y-old man with hard to control HTN, is found to
have renal artery stenosis (RAS).
The following statements about RAS are true
except:
A. 80 % of cases are due to atherosclerosis
B. Fibromuscular dysplasia commonly affects
young men
C. Hypokalemia and metabolic alkalosis may occur
D. Renovascular HTN (RVH) due to Fibromuscular
dysplasia responds to revascularization in the
majority of patients
E. May produce an epigastric bruit
40. Answer 4
A 33-Y-old man with hard to control HTN, is found to
have renal artery stenosis (RAS).
The following statements about RAS are true
except:
A. 80 % of cases are due to atherosclerosis
B. Fibromuscular dysplasia commonly affects
young men
C. Hypokalemia and metabolic alkalosis may occur
D. Renovascular HTN (RVH) due to Fibromuscular
dysplasia responds to revascularization in the
majority of patients
E. May produce an epigastric bruit
41. Question 5
A 35-Y-old woman is admitted to the ER at 8.0 am, after having an
epileptic fit on the station platform.
O/E: She is confused, incontinent in urine and has a temperature of
37 o C. her husband stated that she had a diarrhea for the last few
days and she got a severe headache the evening before. She has
no previous history of epilepsy and she is taking no medications
regularly.
Hb was 8.6 gm/dl, total WBC was 12.000/l. and PLT was 23.000/l.
Retics was 4.6%. Blood film shows occasional fragmented cells.
LDH was 1300 U/l. Electrolytes were normal as well as liver
enzymes. Serum bilirubin was 1.7 mg/dl. Blood urea as 26.4 mg/dl.
Serum creatinine was 1.6 mg/dl.
Which one of the following statements is least likely to be true?
A. The clinical and pathological features may all be related to the
post-ictal state
B. Increased levels of high molecular weight von Willebrand factor
may be found in her blood
C. Enteric infection with E. Coli may be casually related to her
illness
D. The elevated LDH is likely to be of red cell origin
E. Coagulation screening tests in this disorders are usually normal
42. Answer 5
A 35-Y-old woman is admitted to the ER at 8.0 am, after having an
epileptic fit on the station platform.
O/E: She is confused, incontinent in urine and has a temperature of
37 o C. her husband stated that she had a diarrhea for the last few
days and she got a severe headache the evening before. She has
no previous history of epilepsy and she is taking no medications
regularly.
Hb was 8.6 gm/dl, total WBC was 12.000/l. and PLT was 23.000/l.
Retics was 4.6%. Blood film shows occasional fragmented cells.
LDH was 1300 U/l. Electrolytes were normal as well as liver
enzymes. Serum bilirubin was 1.7 mg/dl. Blood urea as 26.4 mg/dl.
Serum creatinine was 1.6 mg/dl.
Which one of the following statements is least likely to be true?
A. The clinical and pathological features may all be related to
the post-ictal state
B. Increased levels of high molecular weight von Willebrand factor
may be found in her blood
C. Enteric infection with E. Coli may be casually related to her
illness
D. The elevated LDH is likely to be of red cell origin
E. Coagulation screening tests in this disorders are usually normal
43. Question 6
A 56-Y-old white man with a history of HTN and IHD, complains
of headache and fatigue. BP was reported as 196/115 and a
normal lab. Evaluation. His physician prescribed him an
ACE-I and instructed him to return in 2-Weeks
The patient is brought to the ER five-Ds later with severe
proximal muscle weakness to the point he cannot rise from
a chair and is experiencing extreme fatigue, nausea and
vomiting.
Without other information available, which of the following
is/are possible?
A. The patient has symptomatic renal failure related to ACE-
Inhibition
B. Life-threatening Hyperkalemia is present
C. This patient has probable Renovascular HTN
D. A, B, and C are correct
E. Only A and C are correct
44. Answer 6
A 56-Y-old white man with a history of HTN and IHD, complains
of headache and fatigue. BP was reported as 196/115 and a
normal lab. Evaluation. His physician prescribed him an
ACE-I and instructed him to return in 2-Weeks
The patient is brought to the ER five-Ds later with severe
proximal muscle weakness to the point he cannot rise from
a chair and is experiencing extreme fatigue, nausea and
vomiting.
Without other information available, which of the following
is/are possible?
A. The patient has symptomatic renal failure related to ACE-
Inhibition
B. Life-threatening Hyperkalemia is present
C. This patient has probable Renovascular HTN
D. A, B, and C are correct
E. Only A and C are correct
45. Question 7
A 68-Y-old man has increasing HTN 3 weeks after an aortic angiogram and
subsequent repair of an abdominal aortic aneurysm. In the hospital, he
received brief courses of several drugs, including cephalosporins,
Cimetidine and heparin. He is currently receiving aspirin and dipyridamole.
Now BP is 170/110 mmHg. Bruits are heard on femoral arteries and there is
some mottling of the lower extremities and subungual petechiae on a lower
extremity nail bed.
Na +=142 mEq/l, and K +=5.1 mEq/l. CL -=104 mEq/l , and HCO3 - = 20
mEq/l. BUN=60 mg/dl, and S.Creat.=3.2 mg/dl. Hematocrit=35%, WBCs = 10.500
/l; PMNs=80 %, Lymphocytes=12%, Eosinophils= 8%.
Urine analysis shows: pH=5.2, protein ++, WBCs= 1-3/HPF, RBCs=10-15/HPF. Wright
stain of urine is positive for eosinophils
Choose the diagnosis most likely to explain the azotemia and HTN in
this patient
A. Nephrosclerosis
B. Atheroembolic disease
C. Drug-induced IN
D. Radio contrast-induced renal disease
E. Postoperative ATN
46. Answer 7
A 68-Y-old man has increasing HTN 3 weeks after an aortic angiogram and
subsequent repair of an abdominal aortic aneurysm. In the hospital, he
received brief courses of several drugs, including cephalosporins,
Cimetidine and heparin. He is currently receiving aspirin and dipyridamole.
Now BP is 170/110 mmHg. Bruits are heard on femoral arteries and there is
some mottling of the lower extremities and subungual petechiae on a lower
extremity nail bed.
Na +=142 mEq/l, and K +=5.1 mEq/l. CL -=104 mEq/l , and HCO3 - = 20
mEq/l. BUN=60 mg/dl, and S.Creat.=3.2 mg/dl. Hematocrit=35%, WBCs = 10.500
/l; PMNs=80 %, Lymphocytes=12%, Eosinophils= 8%.
Urine analysis shows: pH=5.2, protein ++, WBCs= 1-3/HPF, RBCs=10-15/HPF. Wright
stain of urine is positive for eosinophils
Choose the diagnosis most likely to explain the azotemia and HTN in
this patient
A. Nephrosclerosis
B. Atheroembolic disease
C. Drug-induced IN
D. Radio contrast-induced renal disease
E. Postoperative ATN