on 19-Apr-2016 (Tue)

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#exam #nephrology

Question

What are causes of renal artery stenosis?

Answer

• athrosclerosis
• ​fibromuscular dysplasia

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Question

What triggers ADH release?

Answer

• Hypernatremia (osmotic stimulus)
• Non‐osmotic stimuli (inapproriate)
– Low volume states: real or “effective”
– Stress states: surgery, pain
– SIADH states: cancers, drugs, brain or respiratory disease
– Other states: Pregnancy, low cortisol, low thyroid

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Question

hyponatremia rx

Answer

• Restrict fluid/water intake
• Remove underlying cause (ADH)
• If acute and symptomatic → rapid partial correction to reduce cerebral edema (can use hypertonic saline)
• If chronic and severe (<120 mmol/L ) treat slowly as rapid correction can cause devastating brain injury

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Question

hyperkalemia s&s

Answer

• Muscle weakness, stiffness (cells are depolarized)
• ECG changes:
– Small or absent P waves
– Broad QRS
– Peaked T‐waves
• Arrhythmias
• [K+] > 7.0 mmol is life‐threatening

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Question

met acid causes w/ ↑ AG

Answer

**• Lactic acidosis
• Ketoacidosis
--diabetic
--alcoholic
--starvation
• Toxins
– Methanol
– Ethylene glycol
– Salicylates
• Severe chronic kidney disease**

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Question

What is nephrotic syndrome a constellation of?

Answer

Constellation of:
• Hypoalbuminemia
• Edema
• Lipiduria and Hypercholesterolemia
• Proteinuria > 3.5 g/day

Typical Pathology:
• Non‐proliferative Disease (structural abn - glomerulonephropathy)

Nephrotic Syndrome can ONLY be caused by a glomerular disease

No RBC cast

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Question

What is the approach to edema?

Answer

edema = Alterations in Starling (hydrostatic & oncotic) forces:
Increased hydrostatic pressure (Na+ retention)
• Heart failure
• Drugs: Eg. CCBs, NSAIDs, Thiazolidinediones, Minoxidil
Decreased oncotic pressure (hypoalbuminemia)
• Protein loss: nephrotic syndrome, protein losing enteropathy
• Reduced albumin synthesis: liver disease
Increased capillary permeability
• Diabetes
• Malnutrition

Approach: hx, p/e, labs, investigations

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Question

What is going on pathologically with nephrotic syndrome?

Answer

it's a non-proliferative injury to the glomerular basement membrane that causes significant protein (albumin) leakage into the urine

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Question

How do you measure urine protein excretion?

Answer

Screening: (qualitative test)
• Urine dipstick

Quantitative:
• Albumin to Creatinine ratio (ACR)
--Spot sample (First morning specimens most accurate)
• 24 hour urine collection
--gold standard
--Normal value < 150 mg protein excreted per day

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Question

How does proteinuria cause edema?

Answer

• Hypoalbuminemia → increased water and salt retention
--↓ oncotic pressure results in volume depletion, ↓ CO
--activation of RAAS

• Primary defect in the collecting tubule → uncontrolled water and salt retention

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Question

What is the possible mechanism of hypoalbuminemia in nephrotic syndrome?

Answer

--Proteinuria
--not enough replacement from liver synthesis ← TNF & IL-1 may directly suppress hepatic synthesis

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Question

What is the mechanism for hyperlipidemia/lipiduria in nephrotic syndrome?

Answer

• Hepatic lipoprotein synthesis stimulated by decreased oncotic pressure
• Further exacerbated by impaired metabolism and diminished clearance
• Increased risk of atherosclerosis and cardiovascular disease

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Question

Urinalysis of patient with nephrotic syndrome shows [...] and [...]

Answer

Oval fat bodies
fatty casts

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Question

Urinalysis under polarized light of patient with nephrotic syndrome shows [...] with [...] appearance

Answer

Oval fat bodies
Maltese cross

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Question

What are other features of nephrotic syndrome?

Answer

• Hypercoaguable state due to increased urinary loss of anticoagulants antithrombin III, protein C and protein S
• Increased risk of venous thromboembolism Eg. DVT, PE
• 30% of patients have renal vein thrombosis

NB: always be on lookout for these in pt w/ nephrotic syndrome

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Question

What are the causes of nephrotic syndrome?

Answer

3 pathologic causes: (can be primary/secondary to an underlying ds)
--minimal change
--focal segmental glomerulosclerosis (FSGS)
--membranous

2 secondary causes:
--DM
--amyloid/multiple myeloma

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Question

Minimal change disease is the most common cause of [what condition] in [who]

Answer

nephrotic syndrome
children

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Question

What are the main secondary causes of minimal change ds?

Answer

– NSAIDs
– Hodgkin lymphoma

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Question

What can you see on pathology of minimal change ds?

Answer

No difference in appearance from normal glomerulus on light microscopy

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Question

FSGS has worse response to [...] and [...] compared to minimal change and membranous ds

Answer

FSGS has worse response to treatment and poorer prognosis compared to minimal change and membranous ds

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Question

FSGS has worse response to treatment and poorer prognosis compared to [...] and [...]

Answer

FSGS has worse response to treatment and poorer prognosis compared to minimal change and membranous ds

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Question

What do you see on pathology of FSGS?

Answer

Presence of mesangial collapse and sclerosis in some glomeruli (focal) segmental areas

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Question

[...] is the most common cause of nephrotic syndrome in adults

Answer

Membranous ds

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Question

What are the main secondary causes of membranous ds?

Answer

– Malignancy – usually solid tumors Eg. breast, colon
– Autoimmune – SLE
– Infections – Hep B, Hep C, malaria, syphilis
– Drugs – Gold, penicillamine

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Question

What's observed in membranous nephropathy pathology?

Answer

Membranous nephropathy characterized by basement membrane thickening with little or no cellular proliferation on light microscopy

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Question

[...] is the most common cause of secondary nephrotic syndrome in adults

Answer

DM is the most common cause of secondary nephrotic syndrome in adults

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Question

DM is the most common cause of [...] in adults

Answer

DM is the most common cause of secondary nephrotic syndrome in adults

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Question

What are the risk factors of DM?
(which can cause nephrotic syndrome)

Answer

– Uncontrolled hyperglycemia
– Hypertension
– Proteinuria
– Smoking
– Dyslipidemia
– Genetic predisposition

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Question

What is the characteristic kidney bx finding in diabetic nephropathy?

Answer

Kimmelsteil‐Wilson nodules

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Question

What is the rx for nephrotic syndrome?

Answer

Step 1: Treat Symptoms
• Salt restriction and diuretics for edema
• ACEi /ARBs to decrease proteinuria
• Statins for increased cholesterol
• Anticoagulation, if thromboembolism

Step 2: Treat pathological disease
• If secondary process found, treat accordingly
• Otherwise, immunosuppressive medications if indicated: (in truly primary cases)
--Corticosteroids (prednisone) + Other immunotherapy (some other agent)

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Question

What are clues that the renal parenchymal disease is tubulointerstitial?

Answer

– WBCs and WBC casts in the urine
– Variable degree of proteinuria, but usually < 1.5 g
– Evidence of renal tubular dysfunction Eg.hyperkalemia, renal tubular acidosis

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Question

What are acute tubulointerstitial diseases?

Answer

• Acute allergic interstitial nephritis (Eg. to a drug)
• Acute tubular necrosis

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Question

What are chronic tubulointerstitial diseases?

Answer

• Drugs: – Analgesic nephropathy, NSAIDs, Lithium, chemotherapy, antiretrovirals, Chinese herbs
• Chronic obstruction/infection/reflux/stones
• Autoimmune: – Sjogren’s syndrome, sarcoidosis
• Cystic diseases: – Most common, polycystic kidney disease

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Question

What is polycystic kidney ds?

Answer

• Progressive cyst growth and enlargement
• Can lead to hypertension, chronic kidney disease
• Cysts can also bleed, rupture or become infected

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Question

What are extrarenal manifestations of polycystic kidney ds?

Answer

• Cerebral aneurysms
• Cysts in other organs: liver, pancreas
• Valvular heart disease:
– Mitral valve prolapse and aortic regurgitation most common
• Diverticulosis of colon
• Hernia formation (d/t ↑ intra-abdo pressure)

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Question

What are vascular kidney diseases?

Answer

Arteries → renal artery stenosis (atherosclerosis, fibromuscular dysplasia)
Arterioles → atheroembolic ds
Capillaries → thrombotic microangiopathies (thrombotic thrombocytopenic purpura, hemolytic uremic syndrome)
Veins → thrombosis

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Question

How do you classify causes of nephrotic syndrome in peds?

Answer

• First year of life (often genetic)
– Primary
– Secondary
• Older children and adolescents
– Primary
– Secondary

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Question

What are causes of nephrotic syndrome in the first year of life?

Answer

• Primary
– Congenital nephrotic syndrome of the Finnish type (mutation in nephrin gene)
– Mesangial sclerosis (mutation in WT1 gene)
– Associated with other genetic syndromes (multiple gene mutations)
– Minimal change disease after 6 months
• Secondary
– Congenital infections

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Question

What are causes of nephrotic syndrome after the first year of life?

Answer

Primary
– Minimal Change Disease
– Focal Segmental Glomerulosclerosis (some associated with genetic mutations)
– Membranous Nephropathy
– (membranoproliferative glomerulonephritis - nephrotic/nephritic)

Secondary
– Systemic Lupus Erythematosus
– Drugs
– Infections : HIV, malaria
– Lymphomas/leukemias
– Genetic syndrome

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Question

What do you do in an older child/adolescent presenting with minimal change ds nephrotic syndrome?

Answer

If presents w/ typical ft's, start w/ steroid therapy (also allows for specific dx based on response) and don't bx right away

unless has other atypical ft's: (indication for bx) - suggesting non-idiopathic MCNS
--age <1 y or >12y
--+ve fhx
--extrarenal ds (arthritis, rash, anemia)
--chr ds
--sx's d/t intravascular volume expansion (HTN, pulm edema)
--renal failure
--active urine sediment (red blood cell casts)

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Question

What is the initial rx for minimal change neprhotic syndrome (peds)?

Answer

– Prednisone therapy: 60 mg/m2/day with taper over 3-4 months
– Control of Edema
– Low salt diet

Response
– Usually in 2 weeks
– 95% will respond in 4 weeks

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Question

What is the rx of relapses for minimal change nephrotic syndrome (peds)?

Answer

– High dose Prednisone again
– Second line drugs if multiple relapses
• Cyclophosphamide, cyclosporine, tacrolimus, mycophenolate mofetil, rituximab (all have s/e)

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Question

What are complications of therapy for minimal change nephrotic syndrome in kids?

Answer

steroids, cytotoxic drugs, diuretics, etc

NB: what it said in the notes; not sure if means these cause complications

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Question

Children with minimal change nephrotic syndrome often have [...] @ puberty w/ [...]

Answer

long term remission
normal renal function

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Question

What are causes of glomerulonephritis in children?

Answer

Hypocomplementemic (low C3)
– Primary renal disease

• post infectious glomerulonephritis (post strep GN most common)
• membranoproliferative glomerulonephritis
• C3 nephropathy

– Systemic disease

• SLE (main)
• shunt nephritis
• sub acute bacterial endocarditis

Normocomplementemic (normal C3)
– Primary renal disease

• IgA nephropathy
• ANCA + pauci immune GN

– Systemic disease

• ANCA + ds (GPA granulomatosis w/ polyangiitis, MPA microscopic polyangiitis)
• Anti GBM ds (goodpasture ds)
• Henoch Schonlein Purpura

NB: so check for C3 in labs

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Question

What are ft's of post-infectious GN in kids?

Answer

• Evidence of previous infection
– Post Strep is most common
• Nephritic syndrome
• Low C3

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Question

What can cause post strep GN in kids?

Answer

• Strep pharyngitis
– nephritogenic strain
– may be seasonal
– occurs 10-14 days following infection

• Impetigo (skin infection)
– nephritogenic strain
– more frequent in temperate climate
– occurs up to 3 weeks following infection

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Question

Post Strep Glomerulonephritis Pathology

Answer

proliferative GN w/ PMNs

C3 deposits on immunofluorescence

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Question

What are the presentations of post strep GN (peds)?

Answer

– Gross hematuria described as tea coloured or coke like urine
– Mild to moderate edema
– Mild to severe hypertension
– Mild to moderate renal dysfunction
– Hyperkaliemia
– Urinalysis: protein and blood and casts

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Question

What is the rx for post strep GN (peds)?

Answer

• Conservative Treatment of renal failure
– Fluid Restriction
– Potassium restriction
– Phosphate restriction
• Antihypertensives
• Diuretics
• Not an indication for steroids (will usually start to improve w/i a week)

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Question

Post Strep Glomerulonephritis Outcome

Answer

• C3 back to normal by 6-8 weeks
– if persistent hypocomplementemia past 8 weeks consider other diseases
• Spontaneous recovery in more than 95% of children
• No recurrence

=excellent outcome

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Question

What are the 2 major forms of hemolytic uremic syndrome?

Answer

– Typical or Diarrhea positive HUS
• Usually caused by shiga toxin producing E Coli or shigella bacteria
• Most common is E Coli 0157:H7
• Over 90% of cases of HUS in children
– Atypical HUS
• Genetic abnormalities of Complement (treatment with Eculizumab)
• Genetic abnormality DKGE
• Other infections (pneumoccoccus)

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Question

What is typical hemolytic uremic syndrome? What is the classic triad observed?

Answer

• HUS is a disease of younger children presenting with acute kidney injury
• Classic triad
– Microangiopathic hemolytic anemia (anemia can be very severe & transfusions are freq needed)
– Thrombocytopenia (severe w/ very low counts - risk of bleeding)
– Acute Kidney Injury (variable severity from abn urinalysis alone to oligoanuria)
• One of the main causes of acute kidney injury in children <3 years of age

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Question

What are sources of infection of e.coli in diarrhea positive HUS?

Answer

– Ground beef
– Bovine contact
– Unpasteurized milk
– Unpasteurized apple cider
– Some vegetables
– Daycare centres and person/person contacts
– Swimming water

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Question

What is the clinical presentation of HUS (peds)?

Answer

• Prodromal episode of vomiting, followed by bloody diarrhea and abdominal pain
• Later simultaneous occurrence of microangiopathic hemolytic anemia, thrombocytopenia and acute kidney injury

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Question

What is the prevention of HUS?

Answer

• Prevention of risk of infection
– No unpasteurized milk
– Safe water testing practices
– Well cooked hamburgers
– Public Health surveillance of meat
• Once infection has occurred, no successful treatment to prevent progression to HUS

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Question

What is the pathogenesis of HUS?

Answer

• Damage to endothelial cells by the TOXIN is the primary event in the pathogenesis of hemolytic-uremic syndrome → narrowed lumen, thrombus, expanded subendothelial zone (TMA capillary)
• Pathology: the cardinal lesion is composed of arteriolar and capillary microthrombi (thrombotic microangiopathy [TMA]) and red blood cell (RBC) fragmentation

• Kidney: affects glomerular capillaries and small arterioles
• Can occur in other organ capillaries

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Question

HUS rx

Answer

• Symptomatic therapy
– Acute Kidney injury : dialysis when needed
– Blood transfusions for severe anemia
– Platelet transfusions if bleeding or in need of surgical procedure
– Treatment of other organ involvement

• No Specific Therapy
– No evidence to support plasma transfusion/exchange in diarrhea positive HUS
– No definite evidence to support Eculizumab therapy

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Question

HUS outcome

Answer

death to complete recovery (varies)

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Question

What are the types of diuretics?

Answer

• Loop diuretics (block NaK2Cl channels)
– Furosemide, bumetanide, torsemide, ethacrynic acid
• Thiazide diuretics (block NaCl cotransporters)
– Hydrochlorothiazide, chlorthalidone, indapamide, metolazone
• K+ sparing diuretics (Aldosterone antagonists)
– Amiloride, triamterene (ENaC channel)
– Spironolactone (Aldosterone receptor)

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Question

Differentiate CKD from AKI

Answer

• Hx/PEx
– Any chronic diseases
– Any systemic features of acute GN
– Any new medications (recent, herbal, OTC)
– Volume status
• Labs
– Anemia
– Secondary hyperparathyroidism (Ca, PO4, PTH)
– Urinalysis (active sediment)
• Investigations
– Abdominal ultrasound

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Question

Cardiac myocytes form a branching network joined at [...]

Answer

intercalated disks
NB: this is where signal for contraction goes through, allowing for synchronized contraction throughout the heart

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Question

Action potential spreads through the conduction system to the [...] and [...] (myocardial depolarization)

Answer

sarcolemma
T-tubules

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Question

Troponin binds to tropomyosin which inhibits [...] from binding to the [...] filament

Answer

myosin
actin

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Question

[...] are primary fuel source of the heart

Answer

Fatty acids (triglycerides)

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Question

Left ventricular myocytes are arranged [in what fashion] (which allows for coordinated contraction)

Answer

circumferentially in a spiral orientation

NB: Right ventricular myocytes are less structured in organization

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Question

Cardiac valves are lined by [...] and have a [...] structure

Answer

endothelium
tri-layer

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Question

What is the tri-layer structure of cardiac valves?

Answer

 Dense collagenous core (fibrosa) along the outflow surface
--Connected to the valvular supporting structures (heart wall)

 Central core of loose connective tissue (spongiosa)

 A layer rich in elastin on the inflow surface (ventricularis or atrialis depending on which chamber it faces)
--Allows for rapid recoil and prompt closure of the valve

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Question

What are the points of interconnection between systemic and pulmonic circuits?

Answer

 Physiological connections (mostly in fetal life) - R to L shunts
-- Foramen Ovale
-- Ductus Arteriosus

 Pathological connections
-- Interatrial, interventricular septal defects
-- Intrapulmonary malformations (arteriovenous malformations)

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Question

[...] has control over SA node

Answer

Autonomic nervous system

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Question

myocardial depolarization:

[...] can cause disease or sudden death
e.g. Long QT Syndrome

Answer

Aberrant channel activity

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Question

S3 - [...] in diastole d/t [...]
S4 - [...] in diastole d/t [...]

Answer

early, blood hitting wall of ventricle when mitral valve opens

late, stiff ventricle

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Question

Heart and vasculature communicate with brain through [what system] helping to regulate cardiac output and vascular tone

Answer

adrenergic nervous system

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Question

the Sympathetics innervate [...] to increase [...]

the Parasympathetics innervate [...] via vagus nerve to decrease [...]

Answer

both atria & ventricles; HR, AV conduction, irritability of foci

atria; vagus nerve; HR, AV conduction, & irritability

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Question

Most oxygen, nutrients delivered via [...] during [...]

Answer

coronary arteries
ventricular diastole

NB: Left main coronary artery (left anterior descending, circumflex) & Right coronary artery

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Question

Three primary determinants of myocardial performance:

Answer

 Loading conditions (preload, afterload)
 Contractile state of myocardium
 Heart rate

NB: loading conditions & contractile state can affect stroke volume

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Question

What histological changes occur in the heart with aging

Answer

 Increased fibrous tissue in myocardium (increased myocardial stiffness)
 Decreased maximum cardiac output
 Deposition of extracellular amyloid in myocardium
 Increased stiffness, atherosclerosis, calcification of vasculature (aorta, coronary arteries)
 Thickening and calcification of valve cusps

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Question

What is the preload?

Answer

The mechanical load caused by blood on the left ventricular myocardium at the end of diastole, before contraction commences
 In essence, the degree to which the myocardium is stretched before it contracts
 Reflects the venous filling pressure

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Question

What is the afterload?

Answer

The load or resistance against which the left ventricular myocardium has to push in order to eject blood

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Question

What is Starling's law for the heart?

Answer

Stroke volume increases the more stretched the ventricle (up to a certain limit) because the ventricles will also contract harder to pump it all out

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Question

The heart produces [...] which induces loss of Na+ from kidneys, diuresis and vasodilatation

Answer

The heart produces atrial natriuretic peptides which induces loss of Na+ from kidneys, diuresis and vasodilatation

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Question

The heart produces atrial natriuretic peptides which induces [3 things]

Answer

loss of Na+ from kidneys, diuresis and vasodilatation

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Question

The heart is essentially [...] differentiated

Answer

terminally

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Question

Where possible the heart adapts to physiological or pathological stresses through [...] and remodelling of the myocardium present

Answer

hypertrophy
remodelling

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Question

Damage to the heart (e.g. myocardial infarction) results in [2 things]

Answer

scarring and fibrosis

NB: Leading to Loss or reduction of normal cardiac function + Numerous possible pathological sequelae depending
on degree of injury

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Question

What are the mechanisms of cardiac ds?

Answer

 Congenital cardiac disease

 Common underlying mechanisms of acquired
cardiac disease
--Vascular/ischemia
--Infectious/inflammatory/autoimmune
--Tissue stress/trauma

 Uncommon underlying mechanisms of acquired
cardiac disease
-- Endocrine/Metabolic
-- Neoplasia

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Question

What is a cardiac myxoma?

Answer

It's a benign neoplasm that often forms in the left atrium and forms a ball that swings around and causes dmg like a wrecking ball

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Question

What are the functional ds categories?

Answer

Cardiac disease may be classified as:
 Failure of the cardiac pump
 Obstruction to blood flow - Through the heart or To the heart
 Regurgitant blood flow (failure to maintain unidirectional blood flow)
 Shunted blood flow
 Disorders of cardiac conduction
 Rupture of the heart or major vessels

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Question

FAILURE OF THE CARDIAC PUMP (CONGESTIVE HEART FAILURE):
Most commonly due to [...] or may be due to stiffness of the ventricular wall preventing ventricular filling (impaired compliance)

Answer

FAILURE OF THE CARDIAC PUMP (CONGESTIVE HEART FAILURE):
Most commonly due to weak contractions of cardiac muscle (impaired contractility) or may be due to stiffness of the ventricular wall preventing ventricular filling (impaired compliance)

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Question

FAILURE OF THE CARDIAC PUMP (CONGESTIVE HEART FAILURE):
Most commonly due to weak contractions of cardiac muscle (impaired contractility) or may be due to [...]

Answer

FAILURE OF THE CARDIAC PUMP (CONGESTIVE HEART FAILURE):
Most commonly due to weak contractions of cardiac muscle (impaired contractility) or may be due to stiffness of the ventricular wall preventing ventricular filling (impaired compliance)

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Question

FAILURE OF THE CARDIAC PUMP (CONGESTIVE HEART FAILURE) is:
Often an [...] presentation for many forms of [...]

Answer

end-stage
chronic heart disease

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Question

The net result of FAILURE OF THE CARDIAC PUMP (CONGESTIVE HEART FAILURE) is:

Answer

reduced ability or inability to pump blood forwards
-Insufficient blood flow to meet metabolic needs of organs and tissues

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Question

How do physiological mechanisms act to maintain arterial pressure and organ perfusion in CHF (failure of the cardiac pump)?

Answer

 Frank-Starling Mechanism: increase in end-diastolic ventricular volume increases tension in wall and enhances contractility

 Activation of the sympathetic nervous system
- Increase heart rate
- Increase myocardial contractility

 Activation of the renin-angiotensin system

 Myocardial adaptations, including hypertrophy and ventricular remodeling

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Question

The hypertrophied heart is vulnerable to [...]

Answer

decompensation

d/t:
 Increase in size of cardiac myocytes
 No proportional increase in capillary number!
 Oxygen consumption increased in hypertrophied heart but supply of oxygen and nutrients potentially more restricted

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Question

Differential Diagnosis of Cardiac Hypertrophy

Answer

Cardiomyopathic processes e.g. Hypertrophic cardiomyopathy
Volume overload processes e.g. Aortic insufficiency
Pressure overload processes e.g. Essential hypertension
Compensatory processes e.g. Atherosclerotic heart disease
Interstitial infiltrative processes e.g Amyloidosis
Storage disease processes e.g. Pompe Disease
Drugs e.g. Anabolic steroids

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Question

Physiological hypertrophy is:

Answer

increased size of cardiomyocytes without significant end organ damage (i.e. fibrosis)

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Question

Pathological hypertrophy is:

Answer

cardiomyocyte hypertrophy associated with both structural changes and molecular changes

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Question

Cardiac hypertrophy initially [...] but ultimately leads to [...]

Answer

decreases wall stress
decreased myocardial performance

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Question

What increases cardiac work? (4 things)

Answer

1) MI (regional dysfn w/ volume overload)
2) valvular ds (pressure and/or volume overload)
3) HTN (pressure overload)
4) cardiomyopathy (cellular contraction defect or myocarditis)

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Question

[...] → ↑ wall stress → cell stretch → hypertrophy and/or dilatation → systolic/diastolic dysfn

Answer

↑ cardiac work → ↑ wall stress → cell stretch → hypertrophy and/or dilatation → systolic/diastolic dysfn

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Question

↑ cardiac work → [...] → cell stretch → hypertrophy and/or dilatation → systolic/diastolic dysfn

Answer

↑ cardiac work → ↑ wall stress → cell stretch → hypertrophy and/or dilatation → systolic/diastolic dysfn

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Question

↑ cardiac work → ↑ wall stress → [...] → hypertrophy and/or dilatation → systolic/diastolic dysfn

Answer

↑ cardiac work → ↑ wall stress → cell stretch → hypertrophy and/or dilatation → systolic/diastolic dysfn

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Question

↑ cardiac work → ↑ wall stress → cell stretch → [...] → systolic/diastolic dysfn

Answer

↑ cardiac work → ↑ wall stress → cell stretch → hypertrophy and/or dilatation → systolic/diastolic dysfn

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Question

↑ cardiac work → ↑ wall stress → cell stretch → hypertrophy and/or dilatation → [...]

Answer

systolic/diastolic dysfn

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Question

Cardiomyopathy is:

Answer

a term used to describe heart disease resulting from an abnormality in the myocardium

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Question

Cardiac myopathy has multiple different etiologies:

Answer

 Primary cardiomyopathies represent diseases of the myocardium itself

 Secondary cardiomyopathies are other systemic disorders that also cause damage to the myocardium (e.g. Alcoholism, infectious myocarditis, thiamine deficiency, etc.)

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Question

What are the patterns of cardiomyopathy?

Answer

 Dilated cardiomyopathy (including arrhythmogenic right ventricular cardiomyopathy) - mix of genetic & acquired
 Hypertrophic cardiomyopathy - usually genetic (beta myosin chain)
 Restrictive cardiomyopathy - usually acquired (something causing stiffening of myocardium e.g. amyloid)

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Question

What are other causes of myocardial dysfunction or damage?

Answer

 Myocarditis - Infectious, Immune-mediated
 Cardiotoxic drugs - Cancer chemotherapy drugs, lithium, etc.
 Amyloidosis - Cardiac restricted (transthyretin), Systemic amyloidosis

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Question

fluid hemodynamics:
The capillary bed is the site of [...]

Answer

hemodynamic control

NB:
Arteriolar end – hydrostatic pressure predominates
Venular end – oncotic pressure predominates

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Question

fluid hemodynamics:
Exit of fluid at the [...] end is nearly balanced by influx of fluid at the venular end

Answer

arteriolar
venular

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Question

fluid hemodynamics:
Excess interstitial fluid is drained via [...]

Answer

lymphatics

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Question

CAUSES OF EDEMA

Answer

 Increased hydrostatic pressure: - Venous obstruction, congestive heart failure, arteriolar dilatation
 Reduced plasma oncotic pressure: - Cirrhosis, malnutrition, nephrotic syndrome
 Lymphatic obstruction
 Sodium Retention
 Inflammation

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Question

In Subcutaneous edema, Distribution is influenced by [...] and is most pronounced in the [...] parts of the body

Answer

gravity
dependant

NB: it may be the first clue to heart failure

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Question

pulmonary edema is Most commonly seen with [...]

Answer

left ventricular failure

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Question

Brain edema May be [...] or generalized (e.g. encephalitis, CSF outflow obstruction)

Answer

localized (e.g. with abscess or neoplasm)

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Question

Brain edema May be localized (e.g. with abscess or neoplasm) or [...]

Answer

generalized (e.g. encephalitis, CSF outflow obstruction)

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Question

CLINICAL CONSEQUENCES OF EDEMA

Answer

Effects range from merely annoying to fatal

 Subcutaneous edema most significant as a marker of an underlying problem with fluid hemodynamics
 Pulmonary edema can interfere with normal ventilatory function
 Severe brain edema can result in herniation and compression of critical structures

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Question

Obstruction to blood flow can take two forms:

Answer

 Obstruction to flow of blood through the heart (e.g. obstruction of a valve or great vessel)
 Obstruction to flow of blood to the heart (i.e. obstruction of a coronary vessel) - reducing blood supply to the heart when it needs it the most

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Question

Obstruction to blood flow through the heart is frequently due to problems with [...]

Answer

heart valves

E.g. Aortic valve stenosis, Congenital heart valve problems (e.g. Tricuspid atresia, bicuspid aortic valve), Endocarditis

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Question

A stenotic valve cannot open completely, thus hindering [...]

Answer

forward flow of blood

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Question

Valve stenosis can lead to [...] and can also lead to cardiac hypertrophy or potentially pump failure if untreated

Answer

increased work for the heart (pressure overload)

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Question

Valve stenosis can lead to increased work for the heart (pressure overload) and can also lead to [...] or potentially pump failure if untreated

Answer

cardiac hypertrophy

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Question

Valve stenosis can lead to increased work for the heart (pressure overload) and can also lead to cardiac hypertrophy or potentially [...] if untreated

Answer

pump failure

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Question

Obstruction to blood flow through coronary aa → MI
why?

Answer

Development of atherosclerotic plaque +/- thrombus (fixed or variable obstruction)

Occlusive thrombus on plaque (complete obstruction)

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Question

What is the triad of thrombosis?

Answer

hypercoagulability

abnormal blood flow

endothelial injury

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Question

What is the predominant cause of thrombosis?

Answer

Endothelial injury

-Particularly important for arterial or cardiac thrombus formation
-Frequently occurs over atherosclerotic plaques, or at sites of trauma or inflammatory vascular injury (vasculitis)
-May be due to physical disruption of endothelium with exposure of underlying collagen, or endothelial dysfunction

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Question

What types of abn blood flow can lead to thrombosis?

Answer

turbulence
-Contributes to arterial/cardiac thrombosis by promoting endothelial injury/dysfunction
-Also forms countercurrents and local pockets of static blood

stasis
-Major factor in the development of venous thrombi
-hyperviscosity

Turbulence and Stasis:
 Disrupt laminar blood flow
 Allow platelets to come into close contact with endothelium
 Prevent dilution of activated clotting factors
 Promote endothelial cell activation