Lecture 21+22 Flashcards
1
Q
MOA of 1A, 1B, 1C
A
Na channel blocker
2
Q
MOA of class II
A
Beta adrenoceptor blocker
3
Q
MOA of class III
A
K channel blocker
4
Q
MOA of class IV
A
Ca channel blocker
5
Q
what anti arrhythmic act on the SA node
A
Beta blockers (II) IV (Ca channel blockers) digoxin
6
Q
what anti arrhythmic act on the AV node
A
Ca channel blocker (IV) beta blockers (II) digoxin
7
Q
atrial myocyte (anti-arrhythmic)
A
Class IA + 1C
K channel blockers (III)
8
Q
ventricular myocytes (anti-arrhythmic)
A
Na channel blockers (I)
K channel blockers (III)
9
Q
accessory pathways (anti-arrhythmic)
A
Class 1A and K channel blockers (III)
10
Q
what drugs are effective for Ventricular &
supraventricular arrhythmia
A
Class’s IA & IC
K+ channels blockers (III)
11
Q
what drugs are effective for mainly ventricular arrhythmia
A
Lidocaine (IB) & mexiletine (IB)
12
Q
what drugs are effective against mainly
Supraventricular arrhythmias
A
Calcium-channel blockers (IV)
B-blockers (II)
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
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)
15
Q
drugs to prevent thrombosis
A
- heparin- unstable patients who need immediate treatment
2. warfarin- stable patients
16
Q
patho of stable angina
A
- Lumen narrowed by plaque
* Inappropriate vasoconstriction
17
Q
patho of unstable angina
A
- Plaque ruptured
- Platelet aggregation
- Thrombus formation
- Unopposed vasoconstriction
18
Q
patho of variant angina
A
- No overt plaques
* Intense vasospasm
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
20
Q
nitrate examples
A
Isosorbide dinitrate, Isosorbide mononitrate,
Nitroglycerin, Sodium Nitroprusside
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
CA of nitrates
Variant angina
Stable & unstable angina
acute hear failure (nitroglycerin)
26
AE of nitrates
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
when are B blockers not used for angina
variant angina
28
MOA of Ca channel blockers for angina
Coronary & peripheral vasodilatation
| Reducing contractility
29
CA of Ca channel blockers for angina
used in combo with beta blockers sometimes
used for variant angina symptom's
30
treatment for stable angina
acute attacks: rest or nitroglycerin
maintaince: long acting nitrates and beta blocker
ca channel blockers are 2nd line
ranolazine is 3rd line
31
treatment for unstable angina
symptoms relieved by rest or nitroglycerin
In addition, therapy with nitroglycerin & b-blockers
should be considered
32
variant angina treatment
Symptoms respond to nitroglycerin & Ca2+ channel
| blockers
33
clinical features of nephrotic syndrome
* Hematuria (red blood cells and red cell casts in urine)
* Proteinuria (usually subnephrotic range) with or without edema
* Azotemia
* Hypertension
34
IgA Nephropathy (Berger’s Disease)
characterized by the presence of prominent IgA deposits in the mesangial regions and recurrent hematuria, is the most common type of glomerulonephritis worldwide
35
micro for Berger's disease
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
clinical features of Berger's disease
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
Post Streptococcal Glomerulonephritis
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
micros of post strep glomerulonephritis
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
CF of post strep glomerulonephritis
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
Membranoproliferative Glomerulonephritis
best considered a pattern of immune-mediated injury rather than a specific disease characterized by hypocomplementemia
Can be primary (idiopathic) or secondary
41
type I Membranoproliferative Glomerulonephritis
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
Type II Membranoproliferative Glomerulonephritis
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
micro of Membranoproliferative Glomerulonephritis
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
clinical features of Membranoproliferative Glomerulonephritis
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
Rapidly Progressive Glomerulonephritis
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
type I Rapidly Progressive Glomerulonephritis
Anti GBM antibody mediated
* Renal limited
* Cross reacts with alveolar basement membrane Goodpasture Syndrome
linear immuno
47
Type II Rapidly Progressive Glomerulonephritis
Immune complex mediated
```
• Idiopathic
• Post infectious
glomerulonephritis
• IgA glomerulonephritis
• Henoch Schonlein purpura (HSP)
• Lupus nephritis
```
Granular immunofluorescence
48
Type III Rapidly Progressive Glomerulonephritis
ANCA mediated
* Idiopathic
* Wegener’s granulomatosis
* Microscopic polyangiitis
* Churg Strauss syndrome
No immunofluorescence (Pauci immune)
49
histo of Rapidly Progressive Glomerulonephritis
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
CF of Rapidly Progressive Glomerulonephritis
severe injury
| Proteinuria (non-nephrotic), hematuria, red blood cell casts, hypertension, edema, variable degree of oliguria
51
Lupus Nephritis
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
