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CRS > Lecture 21+22 > Flashcards

Lecture 21+22 Flashcards

1
Q

MOA of 1A, 1B, 1C

A

Na channel blocker

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2
Q

MOA of class II

A

Beta adrenoceptor blocker

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3
Q

MOA of class III

A

K channel blocker

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4
Q

MOA of class IV

A

Ca channel blocker

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5
Q

what anti arrhythmic act on the SA node

A 
Beta blockers (II) 
IV (Ca channel blockers)
digoxin
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6
Q

what anti arrhythmic act on the AV node

A 
Ca channel blocker (IV) 
beta blockers (II) 
digoxin
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7
Q

atrial myocyte (anti-arrhythmic)

A

Class IA + 1C

K channel blockers (III)

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8
Q

ventricular myocytes (anti-arrhythmic)

A

Na channel blockers (I)

K channel blockers (III)

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9
Q

accessory pathways (anti-arrhythmic)

A

Class 1A and K channel blockers (III)

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10
Q

what drugs are effective for Ventricular &

supraventricular arrhythmia

A

Class’s IA & IC

K+ channels blockers (III)

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11
Q

what drugs are effective for mainly ventricular arrhythmia

A

Lidocaine (IB) & mexiletine (IB)

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12
Q

what drugs are effective against mainly

Supraventricular arrhythmias

A

Calcium-channel blockers (IV)

B-blockers (II)

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13
Q

what drugs are used for rate control

A

slowing of ventricular rate or negative dromotropic agents

Ca channel blocker
B blocker
digoxin
amiodarone

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14
Q

what drugs are used for rhythm control

A

(induction / maintenance of sinus rhythm)

Class IC antiarrhythmics, (flecainide, propafenone)
Class III antiarrhythmics, (amiodarone, dofetilide)

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15
Q

drugs to prevent thrombosis

A
  1. heparin- unstable patients who need immediate treatment

2. warfarin- stable patients

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16
Q

patho of stable angina

A
  • Lumen narrowed by plaque

* Inappropriate vasoconstriction

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17
Q

patho of unstable angina

A
  • Plaque ruptured
  • Platelet aggregation
  • Thrombus formation
  • Unopposed vasoconstriction
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18
Q

patho of variant angina

A
  • No overt plaques

* Intense vasospasm

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19
Q

patho of angina generally

A

increase HR, contractility, afterload, and preload = increase oxygen consumption = angina

vasospasm, fixed stenosis, thrombus = decreased blood flow = angina

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20
Q

nitrate examples

A

Isosorbide dinitrate, Isosorbide mononitrate,

Nitroglycerin, Sodium Nitroprusside

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21
Q

B blockers used for angina

A

Atenolol, Metoprolol, Propranolol

22
Q

Ca channel blockers for angina

A

Amlodipine, Nifedipine, Diltiazem, Verapamil

23
Q

Na channel blocker used for angina

A

Ranolazine

24
Q

MOA of nitrates

A

Rapid reduction in myocardial O2 demand

vasodilation
anti thrombotic
anti INF

reduce preload and afterload

25
Q

CA of nitrates

A

Variant angina
Stable & unstable angina

acute hear failure (nitroglycerin)

26
Q

AE of nitrates

A

tolerance develops rapidly

headache

high doses: postural hypotension, facial flushing, reflex
tachycardia

cannot have if taking sildenafil ( thus drug inhibits PDE5 thus no relaxation

27
Q

when are B blockers not used for angina

A

variant angina

28
Q

MOA of Ca channel blockers for angina

A

Coronary & peripheral vasodilatation

Reducing contractility

29
Q

CA of Ca channel blockers for angina

A

used in combo with beta blockers sometimes

used for variant angina symptom’s

30
Q

treatment for stable angina

A

acute attacks: rest or nitroglycerin

maintaince: long acting nitrates and beta blocker

ca channel blockers are 2nd line
ranolazine is 3rd line

31
Q

treatment for unstable angina

A

symptoms relieved by rest or nitroglycerin

In addition, therapy with nitroglycerin & b-blockers
should be considered

32
Q

variant angina treatment

A

Symptoms respond to nitroglycerin & Ca2+ channel

blockers

33
Q

clinical features of nephrotic syndrome

A
  • Hematuria (red blood cells and red cell casts in urine)
  • Proteinuria (usually subnephrotic range) with or without edema
  • Azotemia
  • Hypertension
34
Q

IgA Nephropathy (Berger’s Disease)

A

characterized by the presence of prominent IgA deposits in the mesangial regions and recurrent hematuria, is the most common type of glomerulonephritis worldwide

35
Q

micro for Berger’s disease

A

light: Mesangioproliferative pattern segmental mesangial widening and endocapillary proliferation

immuno: Mesangial deposition of IgA often with C3 and lesser amounts of IgG or IgM
Early complement components are usually absent

electron: Electron -dense deposits predominantly in the mesangium

36
Q

clinical features of Berger’s disease

A

Most common in children and young adults

Episodes of gross hematuria (associated with viral respiratory illness or GI illness)

Persistent microscopic hematuria between these episodes

Usually non-nephrotic range proteinuria (<3.5gm/day)

Normal C3/C4 levels

37
Q

Post Streptococcal Glomerulonephritis

A

cluster of diseases characterized histologically by diffuse proliferation of glomerular cells associated with influx (exudation) of leukocytes, typically caused
by immune complexes

eito:
Most common underlying infections: certain nephritogenic strains of group A βhemolytic streptococci, more than 90% of cases being traced to types 12, 4, and 1
Throat infection- pharyngitis, skin infection- impetigo

Initially: subendothelial immune complex deposits → pathogenesis of nephritic syndrome
Later: through unknown mechanisms → subepithelial deposits form → present at time of biopsy

38
Q

micros of post strep glomerulonephritis

A

light: The increased cellularity is caused both by
proliferation and swelling of endothelial and mesangial cells and by infiltrating neutrophils (1) and monocytes

immuno: Granular deposits of IgG and C3 in the
mesangium and along capillary walls

electron: Electron dense immune complex deposits in the subepithelial space called “humps” (2)
Mesangial deposits may also be seen

39
Q

CF of post strep glomerulonephritis

A

Manifests usually 10 days following pharyngitis and 3 weeks following impetigo (late period of antibody formation)

More common in children (6-10 years age)

long term could be renal damage

40
Q

Membranoproliferative Glomerulonephritis

A

best considered a pattern of immune-mediated injury rather than a specific disease characterized by hypocomplementemia

Can be primary (idiopathic) or secondary

41
Q

type I Membranoproliferative Glomerulonephritis

A

Most common type of MPGN ( can be idiopathic or secondary)
IgG- immune complex mediated
Classical pathway activated

Immune complex deposition in subendothelial and mesangial spaces → inflammation and damage to GBM

42
Q

Type II Membranoproliferative Glomerulonephritis

A

Very rare; also called Dense Deposit Disease
Non IgG, non immune complex mediated
Alternate pathway activated

Associated with specific genetic mutations and/or autoantibodies to alternate complement pathway factors or regulatory factors of alternate complement pathway

Circulating autoantibody termed C3 nephritic factor
(C3NeF) binds the alternative pathway C3 convertase
and protects it from inactivation. This favors persistent
C3 activation and hypocomplementemia

43
Q

micro of Membranoproliferative Glomerulonephritis

A

light: showing mesangial cell proliferation, basement membrane duplication, leukocyte infiltration, and
accentuation of lobular architecture

Glomerular capillary wall often shows a double contour (silver / PAS)

This “splitting” of the GBM is due to extension of processes of mesangial and inflammatory cells into the peripheral capillary loops and deposition of
mesangial matrix as well as subendothelial immune complexes

immuno:
type I: IgG and C3 are deposited in a granular pattern, and early complement components (C1q and C4) are often also present.

type II: C3 is present in irregular granular or linear foci in the basement membranes. IgG is usually absent, along with components of the classical pathway of
complement activation (such as C1q and C4)
44
Q

clinical features of Membranoproliferative Glomerulonephritis

A

Usually presents before age 30 in one of 4 ways:

  1. Hematuria or proteinuria discovered on urinalysis
  2. Acute nephritic syndrome with hematuria, HTN and edema
  3. Recurrent episodes of gross hematuria
  4. Insidious onset of edema and nephrotic syndrome

Most progress to ESRD within 10-15 years

45
Q

Rapidly Progressive Glomerulonephritis

A

Characterized by relatively rapid and progressive loss of renal function associated with severe oliguria and signs of nephritic syndrome; if untreated, death from renal failure may occur within weeks to months

histo:
• Presence of crescents in most of the glomeruli, hence the name crescentic glomerulonephritis
• Produced predominantly by the proliferation of the epithelial cells lining the Bowman capsule and by the infiltration of monocytes and macrophages

46
Q

type I Rapidly Progressive Glomerulonephritis

A

Anti GBM antibody mediated

  • Renal limited
  • Cross reacts with alveolar basement membrane Goodpasture Syndrome

linear immuno

47
Q

Type II Rapidly Progressive Glomerulonephritis

A

Immune complex mediated

• Idiopathic
• Post infectious
glomerulonephritis
• IgA glomerulonephritis
• Henoch Schonlein purpura (HSP)
• Lupus nephritis

Granular immunofluorescence

48
Q

Type III Rapidly Progressive Glomerulonephritis

A

ANCA mediated

  • Idiopathic
  • Wegener’s granulomatosis
  • Microscopic polyangiitis
  • Churg Strauss syndrome

No immunofluorescence (Pauci immune)

49
Q

histo of Rapidly Progressive Glomerulonephritis

A

light: silver stain: can see necrosis and crescent formation
proliferation of glomerular epithelial cells, migration of macrophages into urinary space and fibrin deposition due to escape of procoagulant factors (more fibrotic)

electron:
Electron microscopy discloses deposits in those cases due to immune complex deposition

Regardless of type, electron microscopy may show wrinkling and disruption of basement membranes

50
Q

CF of Rapidly Progressive Glomerulonephritis

A

severe injury

Proteinuria (non-nephrotic), hematuria, red blood cell casts, hypertension, edema, variable degree of oliguria

51
Q

Lupus Nephritis

A

an autoimmune disease involving multiple organs, characterized by a vast array of autoantibodies, particularly antinuclear antibodies (ANAs), in which
injury is caused mainly by deposition of immune complexes and binding of antibodies to various cells and tissues

6 clinical domains of symptoms involving most systems

will have a full house auto-antibody pattern

CRS (16 decks)

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