Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CRS > Lecture 17+18+20 > Flashcards

Lecture 17+18+20 Flashcards

1
Q

all patients with systolic HF take?

A

ACEi + Beta blocker + diuretic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

drugs types for diastolic HF

A

diuretics
ACEi / ARB
ca channel inhibitors
beta blockers

DO not use positive inotropes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

PDE III inhibitor examples

A

Inamrinone and Milrinone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

treatment for abnormal automaticity

A

decrease the slope of phase 4 depolarization

raise the threshold of discharge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

treatment for re-entrant circuits

A

slow conduction

increase the refractory period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

treatment for afterdepolarizations

A

slowing conduction

increase the refractory period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Class II anti-arrhythmic drugs

A

Beta blockers (Ca)

Propranolol, metoprolol, esmolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Class III anti-arrhythmic drugs

A
  • inhibitors of repolarization (K+)

Amiodarone, sotalol, dofetilide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Class IV anti-arrhythmic drugs

A

calcium channel blockers (Ca2+)

Verapamil, diltiazem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

miscellaneous anti-arrhythmic drugs

A

Digoxin, adenosine, magnesium, atropine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Class IA MOA

A

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

prolonged repolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Quinidine

A

Class IA anti-arrhythmic

CA: Suppression of supraventricular and ventricular
arrhythmias

Inhibits CYP 2D6, 3A4 & P-glycoprotein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

contraindications of Quinidine

A

cannot use in those with Heart block

caution in those with heart issues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions