This document provides information on managing renal failure in primary care. It presents a case study of a 46-year-old woman with chronic kidney disease due to uncontrolled diabetes and hypertension. Key steps in management include controlling blood pressure and diabetes, addressing complications like anemia and bone disease, and referring to nephrology if glomerular filtration rate drops below 30 or complications require treatment. The take-home message is that lifestyle modification, monitoring for complications, and early nephrology referral can help slow chronic kidney disease progression.
Define Chronic Renal Failure.
Mention the main causes of Chronic Renal Failure.
Know the signs and symptoms of renal failure.
Know the treatment options of CRF
Know new definition of CKD
Define Chronic Renal Failure.
Mention the main causes of Chronic Renal Failure.
Know the signs and symptoms of renal failure.
Know the treatment options of CRF
Know new definition of CKD
Chronic kidney disease (CKD) consists of a spectrum of different pathophysiologic processes associated with abnormal kidney function, and a progressive decline in glomerular filtration rate (GFR).
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Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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Renal failure
1. Renal Failure
in the Primary Care setting
1
Hasan Ismail
PGY III – Family Medicine
Lebanese University
2. Objectives
• To identify the role of the Family Physician in
the management of CKD
• To be aware of referral indications
• To be able to treat and follow most of the CKD
complications
2
3. • A 46-year-old woman - First visit
• CC :Decreased urinary output for 5 months with
a foamy appearance.
• Swelling in both legs
• non bloody, non bilious emesis a few times a
week.
3
Case scenario 1
4. • Diet: “I eat the best I can for what I afford but
often have very little appetite”
4
• Diabetes since 10 years ago and has been taking
insulin for 2 years.
• She does not check her sugars at home because
she does not like to "stick" herself.
5. • Obese
• Her temperature is 37.2°C, her heart rate is
• 108 beats/min, her blood pressure is 198/105 mm
Hg, her respiration is 19 breaths/
• min, and her oxygen saturation is 94% on room air.
• (HEENT) examination reveals periorbital edema.
• Her skin is hyperpigmented on both lower
extremities.
5
6. • Tachycardia with an S1, S2, S4 gallop, Vesicular
breath
• No jugular venous distension and no carotid
bruits.
• Abdomen is nontender, with no bruits or
masses palpated.
• The lower extremities reveal pitting pretibial
edema with a pit recovery time less than 40
seconds.
6
7. Labs
• Urinalysis
Hyaline casts
3+ proteinuria
Glucose
negative for ketones.
• Her hemoglobin is 10.9 g/dl and her hematocrit is
32% with a mean corpuscular volume (MCV) of
82.3 g/dl.
7
8. Case 1 Summary
• This is a 46-year-old woman with chronic kidney
disease (CKD). She has a history of uncontrolled
diabetes and currently has uncontrolled
hypertension.
• She presents with periorbital edema, long-
standing lower-extremity edema, an S4 and
central obesity.
• The urinalysis shows hyaline casts,
• 3+ proteinuria and glucose, negative ketones, and
hemoglobin 10.9 g/dL with an MCV of82.3 g/dL.
8
12. • Further history to identify and remove any
offending agents (such as nonsteroidal anti-
inflammatory drugs [NSAIDs])
• Control of blood pressure and diabetes
• May require dialysis if she develops
complications such as pulmonary edema,
severe hyperkalemia, or anuria
12
13. • A significant reduction in urine output requires
immediate evaluation of creatinine function and
volume status.
• Volume status is assessed by skin turgor, mucous
membranes, specific gravity in the urinalysis,
and orthostatic blood pressure.
• A low volume status with an elevated creatinine
requires that the patient be given IV fluids to see
if there can be any recovery of kidney function.
13
14. • The patient's uncontrolled diabetes and
hypertension predispose her to kidney
damage.
• Another common offender is a patient with
this history who is taking NSAIDs.
• This will increase the patient's already high
risk of damage.
14
15. Etiologies
• DM, HTN, and glomerulonephritis.
• Diabetic kidney disease occurs in 30% to 40% of
type I DM, in 25% of type II DM, and in 24% of
HTN patients.
• 20% to 60% of DM patient are HTN !
• Many patients present at a later stage of CKD
and it is then difficult to determine the etiology 15
17. • Progressive destruction of nephrons;
• GFR will drop gradually, and plasma Cr
values will approximately double, with
50% reduction in GFR and 75% loss of
functioning nephrons mass.
• Hyperkalemia usually develops when
GFR falls to <20 to 25 mL/min
17
19. • USPSTF 2012
- Insufficient evidence to recommend for or against
routine screening.
• ACP 2013, AAFP 2014
- Do not screen adults unless they have symptoms
or risk factors.
- Adults taking an ACE inhibitor or ARB should not
be tested for proteinuria, regardless of diabetes
status.
19
* USPSTF. Chronic Kidney Disease (CKD): Screening. 2012.
** AAFP Clinical Recommendations: Chronic Kidney Disease. 2014.
Ann Intern Med. 2013;159(12):835
20. • NICE 2014
- Monitor glomerular filtration rate (GFR) at least
annually in people prescribed drugs known to be
nephrotoxic (calcineurin inhibitors, lithium, or
nonsteroidal anti-inflammatory drugs (NSAIDs)..)
- Screen renal function in people at risk for CKD
(DM, HTN, CVD, structural renal disease,
nephrolithiasis, BPH, multisystem diseases with
potential kidney involvement, stage 5 CKD or
hereditary kidney disease, or personal history of
hematuria or proteinuria
20Early identification and management of chronic kidney disease in adults in primary and secondary care. London (UK):
NICE; 2014
23. Definition
≥3 mo w/ GFR <60 mL/min/1.73 m2
or
signs of kidney damage:
Proteinuria/albuminuria, pathology on renal
biopsy/imaging
23
Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 clinical practice
guideline for the evaluation and management of chronic kidney disease. Kidney Int Suppl. 2013; 3(1): 1-150.
25. Albuminuria Stage
25
based on albuminuria (mg/d) or
spot urine Alb/Cr (mg) ratio (ACR):
• A1: nl or mildly ↑ (ACR <30)
• A2: mod ↑ [formerly microalbuminuria]
(ACR 30–299)
• A3: or severely ↑ [formerly macroalbinuria]
(ACR ≥300)
(Kid Int 2013;3:19)
26. Geriatric Considerations
• GFR normally decreases with age, despite
normal creatinine (Cr).
• Adjust renally cleared drugs for GFR in the
elderly.
26
27. Pediatric Considerations
• CKD definition is not applicable for children <2
years because of lower GFR even when
corrected for body surface area.
• Calculated GFR based on serum Cr is used in
this age group.
27
28. Pregnancy Considerations
• Renal function in CKD may deteriorate during
pregnancy.
• Cr >1.5 and hypertension (HTN) are major risk
factors for worsening renal function.
• Increased risk of premature labor, preeclampsia,
and/or fetal loss
• ACE inhibitors and angiotensin receptor blockers
(ARBs) are contraindicated due to teratogenicity.
• Use diuretics with caution
28
29. Assessment : History taking
Patients with CKD stages 1 to 3 are usually
asymptomatic; can present with:
• Oliguria, nocturia, polyuria, hematuria, change
in urinary frequency
• Bone disease
• Edema, HTN, dyspnea 29
33. Evaluation
• Underlying causes may be ascertained through
clinical presentation, symptomatology, and past
medical and family history.
• ANA, antiphospholipid antibodies, C3, C4,
erythrocyte sedimentation rate (ESR) and/or C-
reactive protein (CRP) (looking for lupus
nephritis)
33
34. • Hepatitis panel and HIV test (looking for
infectious etiologies)
• Serum and urine protein electrophoresis
(looking for multiple myeloma) for those
patients older than age 35
• Hemoglobin A1c, fasting blood sugar, and
analysis of urine sediment.
34
36. • Renal biopsy, if not contraindicated by
comorbidities, is indicated in patients with
unknown etiology after history and laboratory
evaluation if parenchymal disease is suspected,
or if treatment or prognosis will be based on the
biopsy.
• However biopsy is contraindicated if bilateral
small kidneys are seen on imaging, as there is a
low likelihood of improving outcome due to the
presence of late-stage disease.
36
44. ACEI or ARB
• 1st-line/renoprotective in all CKD
• tolerate 25% ↑ in Cr and K <5.5; no benefit of
ACEI + ARB combined and associated with
adverse outcomes
• 2nd-line agents include loop diuretics (if edema
present) or diltiazem/verapamil
(↓ proteinuria; antiproteinuric effect not seen
with amlodipine)
44NEJM 2004;351:1952
NEJM 2013;369:1892
47. Renal replacement therapy
• Includes HD, PD, transplant
• Clinical decision; consider when eGFR 5–10 &
sx of uremia/fluid overload.
• No mortality benefit to early initiation of
dialysis & no difference in CV events,
infection, HD complications
47
(CJASN 2011;6:1222)
(IDEAL, NEJM 2010;363:609)
49. Anemia
• Hemoglobin should be measured at least
annually in patients with stage 3 CKD, and
more frequently as renal function declines.
• There is no role for measurement of serum
erythropoietin level in the primary care
setting.
• Goal Hgb 10–11 g/dL
• correct iron deficiency before starting
epoetin/ darbepoetin
49
(NEJM 2009;361:2019)
Kidney Disease: Improving Global Outcomes (KDIGO) Anemia Work Group. KDIGO clinical
practice guideline for anemia in chronic kidney disease. Kidney Int Suppl. 2012; 2(4): 279-335.
50. Bone Disease
• ↓ GFR → ↑ PO4, ↓ Ca, ↓
• PO4 binder (calcium acetate, sevelamer,
lanthanum) if ↑ PO4
• 1,25-(OH) vit D (calcitriol, paricalcitol) if ↑
PTH
50(AJKD 2009;53:408)
(NEJM 2010;362:56;1312)
51. • Volume overload/edema: <2 g/d Na
restriction + diuretics
• Metabolic acidosis : treat w/ sodium
bicarbonate or citrate to HCO3 goal of 23–29
mEq/L; 1 tsp baking soda ≈ 6 tabs of Na-HCO3
≈ 50 mEq HCO3
51
(JAm Soc Nephrol 2015;26:515; Kidney Int 2010;78:303)
52. Nephrology referral
• Early referral associated with ↓ mortality.
• Refer if:
52(Am J Med 2007;120:1063)
• eGFR <30, stage 4/5 CKD;
• DM w/ mod albuminuria
(30–299 mg/d)
• Any UACR ≥300 mg/g
• ? Etiology
• rapidly ↓ GFR
• Complications of CKD
requiring Rx (i.e., Epo, PO4
binders, vit D)
• Hyperkalemia
• Resistant HTN
• Recurrent nephrolithiasis
• Suspicion of hereditary CKD
53. TAKE HOME MESSAGE
• Lifestyle Modification is always essential
• Never Hesitate to refer
• Tell the patient that his disease is irreversible
but can be slowed down
• Never miss the complications
53