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CRS > Lecture 17+18+20 > Flashcards

Lecture 17+18+20 Flashcards

1
Q

all patients with systolic HF take?

A

ACEi + Beta blocker + diuretic

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2
Q

drugs types for diastolic HF

A

diuretics
ACEi / ARB
ca channel inhibitors
beta blockers

DO not use positive inotropes

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3
Q

PDE III inhibitor examples

A

Inamrinone and Milrinone

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4
Q

MOA of PDE inhibitors

A

Inhibit myocardial cAMP PDE activity → increased cAMP
levels

reduce preload and afterload
increase AV conduction slightly

used for short-term HF treatment

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5
Q

dopamine

A

stimulates dopaminergic and adrenergic

• Lower doses = mainly dopaminergic stimulating
(produce renal and mesenteric vasodilation)
• Higher doses = both dopaminergic & b1 stimulating
(produce cardiac stimulation & renal vasodilation)
• Large doses = stimulate a receptors
(vasoconstriction)

used for: cardiogenic shock

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6
Q

Dobutamine

A

At therapeutic levels the stimulation of b1 -receptors
predominate

potent inotropic effect and mild vasodilation

Used to increase cardiac output in acute management
of heart failure

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7
Q

glucagon

A

Stimulates adenylyl cyclase to produce increased cAMP (by binding to GPCR), leading to potent inotropic and chronotropic effects

produces similar effect as beta agonists

Used as a cardiac stimulant in management of severe
cases of b-blocker over dosage

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8
Q

myocardial AP phases

A

phase 0: rapid upstroke and depolarization
Na channels open (Na into cell)

phase 1: initial repolarization
Na channels close, and K open ( K goes out)

phase 2: Plateau
voltage sensitive Ca channels open
slow inward current (balances with K)

phase 3: repolarization
Ca channels close
K channels open (outward)

phase 4: resting potential
increase depolarization due to increase Na permeability

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9
Q

pacemaker AP

A

phase 0: upstroke
Ca channels open (slow velocity)

phase 3:
Ca channels inactivate; increase in K activation

phase 4:
slow repolarization due to If

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10
Q

treatment for abnormal automaticity

A

decrease the slope of phase 4 depolarization

raise the threshold of discharge

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11
Q

treatment for re-entrant circuits

A

slow conduction

increase the refractory period

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12
Q

treatment for afterdepolarizations

A

slowing conduction

increase the refractory period

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13
Q

Class I anti-arrhythmic drugs

A

class I are fast channel blockers for Na

IA: Quinidine, procainamide, disopyramide
(IB) Lidocaine, mexiletine
(IC) Flecainide, propafenone

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14
Q

Class II anti-arrhythmic drugs

A

Beta blockers (Ca)

Propranolol, metoprolol, esmolol

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15
Q

Class III anti-arrhythmic drugs

A
  • inhibitors of repolarization (K+)

Amiodarone, sotalol, dofetilide

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16
Q

Class IV anti-arrhythmic drugs

A

calcium channel blockers (Ca2+)

Verapamil, diltiazem

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17
Q

miscellaneous anti-arrhythmic drugs

A

Digoxin, adenosine, magnesium, atropine

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18
Q

Class I MOA

A

block fast inward Na channels

decrease Na entry; slow raise of phase 0
cause decrease in excitability

Use/state dependence = cells discharging at
abnormally high frequency are preferentially blocked

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19
Q

Class IA MOA

A

slow rate the change in phase 0
prolong phase 3 (inhibit K)

prolonged repolarization

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20
Q

Quinidine

A

Class IA anti-arrhythmic

CA: Suppression of supraventricular and ventricular
arrhythmias

Inhibits CYP 2D6, 3A4 & P-glycoprotein

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21
Q

AE of Quinidine

A 
Arrhythmias (torsades de pointes)
SA & AV block or asystole
Nausea, vomiting & diarrhea (30-50%)
Thrombocytopenic purpura
Cinchonism

toxic dose = tachy

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22
Q

contraindications of Quinidine

A

cannot use in those with Heart block

caution in those with heart issues

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23
Q

MOA of procainamide

A

Similar actions to quinidine
• Blockade of Na+ channels in activated state
• Blockade of K+ channels
• Antimuscarinic properties

CA: Suppression of supraventricular and ventricular
arrhythmias

metabolized by CYP2D6
Partly acetylated to N-acetylprocainamide (NAPA) which prolongs duration of action potential

24
Q

AE of procainamide

A

Reversible lupus-like syndrome (25-30%)

Toxic doses: asystole, induction of ventricular
arrhythmias

CNS effects (depression, hallucination, psychosis)

Weak anticholingeric effects

Hypotension

more prevalent in chronic use

25
Q

contra of procainamide

A

hypersensitivity, SLE, heart issues (heart block)

26
Q

MOA of Disopyramide

A 
Strong negative inotropic effect (> quinidine &
procainamide)
Strong antimuscarinic properties
causes peripheral vasoconstriction
Blocks K+ channels

CA: Suppression of supraventricular and ventricular
arrhythmias

27
Q

AE of disopyramide

A

Pronounced negative inotropic effects
Severe antimuscarinic effects

May induce hypotension & cardiac failure without preexisting myocardial dysfunction

28
Q

pathogenesis of nephrotic syndrome

A

damage to glomerular cells which then increases the permeability of the capillaries to proteins

loss of proteins leads to a decreased plasma oncotic pressure… which then leads to the loss of fluid

edema and increased lipoproteins

29
Q

risks of having membranous nephropathy

A

thrombosis: can be venous or arterial

patho:
1. Hypercoagulability due to Urinary loss of endogenous anticoagulants (anti thrombin III)

Hypoalbuminemia → stimulation of protein synthesis in liver → increased production of coagulation factors

Intravascular volume depletion → increased blood viscosity

  1. Endothelial dysfunction due to pro inflammatory cytokines
30
Q

symptoms of nephrotic syndrome

A

heavy proteinuria
edema
lipiduria
hyperlipidemia

infection and embolism

31
Q

Minimal Change Disease

A

benign disorder is characterized by diffuse effacement of foot processes of visceral epithelial cells (podocytes)

most common cause of nephrotic syndrome in children (2-6)
can sometimes follow a respiratory infection or immunization

eitopath:
some immune dysfunction that results in the elaboration of factors (“glomerular permeability factors”) that damage visceral epithelial cells and cause proteinuria
no immune deposits are seen

32
Q

histo of minimal change disease

A

electron microscopy = will see effaced/ fused foot processes

light = everything looks norm

immuno = no depositions

33
Q

clinical features of minimal change disease

A
  • Disease typically manifests with abrupt development of the nephrotic syndrome in an otherwise healthy child
  • No hypertension
  • Renal function is preserved in most of these patients
  • Periorbital edema and generalized edema (anasarca)
  • Protein loss usually is confined to smaller plasma proteins, chiefly albumin (selective proteinuria)
  • Prognosis for children with this disorder is favorable – no tendency to develop into a chronic renal failure/end stage kidney disease
  • More than 90% of children respond to a short course of corticosteroid therapy
34
Q

Focal Segmental Glomerulosclerosis

A

can be primary (idiopathic) or secondary

primary = most common cause of nephrotic syndrome
disorder of the podocytes

secondary:
HIV, obesity, cancer, drug use

35
Q

patho of secondary FSGS

A

reduction in renal mass due to a renal disease

will lead to compensatory hypertrophy and hyperfiltration

will have Intraglomerular hypertension

Focal and segmental sclerosis in glomeruli

36
Q

micro of FSGS

A

light:
Collapse of capillary loops, increase in matrix, and
segmental deposition of plasma proteins along the
capillary wall

immuno:
Negative/ or non-specific granular deposits of IgM and
C3

electron:
Diffuse effacement of foot processes, and there may also be focal detachment of the epithelial cells and denudation of the underlying GBM

37
Q

Clinical features that differ MCD from FSGS

A
  1. Higher incidence of microscopic hematuria, reduced GFR (renal insufficiency) and hypertension
  2. Proteinuria is more often non-selective (more than just albumin)
  3. Poor response to corticosteroid therapy
  4. Progression to chronic kidney disease (50% develop end stage renal disease within 10 years

proteinuria:
insidious in onset
non-selective
more than 3.5

38
Q

Membranous Nephropathy

A

characterized by diffuse thickening of the glomerular
capillary wall due to the accumulation of deposits containing Ig along the subepithelial side of the basement membrane

epi: 
30-50
more common in males 
most common cause of nephrotic syndrome in elderly
really rare in kids

etio: most cases are primary
Autoimmune disease caused in most cases by antibodies to a renal autoantigen; most commonly PLA2R (phospholipase A2 receptor) on podocytes

secondary:
1. endogenous (SLE, cancer, other Autoimmune conditions)

  1. exogenous
    drugs and infections
39
Q

patho of membranous nephropathy

direct and indirect?

A
  1. antigen-antibody reaction
  2. complement activation
  3. insertion of MAC into membrane

can be direct or indirect damage

direct:
• Alteration of cytoskeleton
• Effacement of foot processes
• Detachment of podocyte

indirect:
• Activation of epithelial and mesangial cells
• Proteases, oxidants, cytokines
• Stimulation of GBM growth (“spikes”)

either way it leads to increased permeability of the BM
massive proteinuria

40
Q

histo of membranous nephropathy

A

light: thickening of the BM
silver stain: spike and dome appearance

immuno:
Granular IgG and C3 deposits around the glomerular basement membrane

41
Q

clinical features of membranous nephropathy

A

nephrotic syndrome, microscopic hematuria (50%), hypertension

some have remission; can develop ESRD or thrombosis

42
Q

Diabetic Nephropathy

A

Renal disease follows cardiac causes (myocardial infarction) of mortality in patients with diabetes mellitus

due to the side effects of hyperglycemia

can see:

  1. Glomerular lesions
  2. Renal vascular lesions, principally arteriolosclerosis
  3. Pyelonephritis (tubules and interstitium), including necrotizing papillitis
43
Q

patho of diabetic nephropathy

A

systemic hyperglycemia

leads to increased matrix formation, increased type IV collagen, and hyperfiltration

44
Q

histo of diabetic nephropathy

A
  1. GBM thickening (identified on EM first)
  2. Mesangial widening
  3. Tubular BM thickening

Kimmelstiel-Wilson nodules will be seen
can see ischemia
hyaline arteriosclerosis

45
Q

NODULAR GLOMERULOSCLEROSIS

A

Distinctive glomerular lesion characterized by ball-like deposits of a laminated matrix in the periphery of the glomerulus
the nodules are PAS +
can be seen in those with chronic DM

kidneys will be granular and contracted

46
Q

clinical features of diabetic nephropathy

A

initially the hyperglycemia just leads to hyperfiltration
(increased GFR)

after a while microalbuminuria occurs

after there is persistent & progressive proteinuria, hypertension, highly variable decline in GFR 1-24 ml/min/year

47
Q

renal amyloidosis

A

kidney will appear to be normal color and shape
in extreme cases they might be smaller

micro:
Amyloid deposited primarily in the glomeruli
Interstitial peritubular tissue, arteries, and arterioles are also affected
will see deposits along the BM

48
Q

CF of renal amyloidosis

A

Most common renal presentation: nephrotic syndrome
Renal insufficiency is present in 50% at time of Diagnosis.
Electrolyte abnormalities (Fanconi syndrome)

49
Q

Nephrotic syndrome

A

Clinical entity due to glomerular disease characterized by
• Heavy proteinuria (>3.5 g/day)
• Hypoalbuminemia and severe edema
• Hyperlipidemia and lipiduria (lipid in urine)

50
Q

Acute kidney injury

A

Rapid decline of GFR (within hours to days)
Dysregulation of fluid and electrolyte balance
Retention of metabolic wastes

51
Q

Chronic kidney disease

A

Reduced GFR that it persistently less than 60 mL/minute/1.73 sq. m for at least 3 months from any cause and/or persistent albuminuria

52
Q

End stage renal disease

A

GFR is less than 5% of normal

This is the terminal stage of uremia

53
Q

Renal tubular defects

A

Polyuria (excessive urine formation) and nocturia
Electrolyte disorders
Disorders directly affecting tubules or cause defects in specific
tubular functions (inherited or acquired)

54
Q

Urinary tract infections

A

Bacteriuria and pyuria

May infect kidney (pyelonephritis) or bladder (cystitis)

55
Q

Nephrolithiasis (renal stones)

A

Spasms of severe pain (renal colic) and hematuria

56
Q

Nephritic syndrome

A

Acute in onset; characterized by Grossly visible hematuria or dysmorphic RBCs and red cell casts in urine

Reduced GFR, mild to moderate proteinuria and hypertension

CRS (16 decks)

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