Brainscape's Knowledge GenomeTM

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


See full index

CRS > Lecture 23+24 > Flashcards

Lecture 23+24 Flashcards

1
Q

aspirin

A

cyclooxygenase inhibitor

Thromboxane A2 causes platelets to degranulate and aggregate.

Aspirin inhibits TXA2 synthesis by irreversible
acetylation of the enzyme COX

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

uses of aspirin

A

reduce risk of stroke
reduce mortality in those with suspected MI
reduce risk of death and MI in patients with previous MI or unstable angina
To reduce risk of MI and sudden death in patients
with stable ischemic heart disease

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

examples of ADP receptor blockers

A

Clopidogrel, ticagrelor, prasugrel, and cangrelor

Ticagrelor and cangrelor bind to the P2Y12
receptor reversibly.

Clopidogrel and prasugrel bind irreversibly

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

MOA of ADP receptor blockers

A

ADP is a mediator of platelet aggregation
These drugs are antagonists of the P2Y12 receptor.
Blockade of the P2Y12 receptor increases cAMP.
Therefore, they reduce platelet aggregation

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

Clopidogrel

A

Clopidogrel is a prodrug converted to an active
metabolite, mainly by CYP2C19

cannot use along with omeprazole for long term ( A CYP2C19 inhibitor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Uses of ADP receptor blockers

A

• Treatment of acute coronary syndromes (ACS).
• Preventive treatment of patients at risk of thromboembolism, myocardial infarction or
stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Dipyridamole

A

phosphodiesterase inhibitor

used for stroke prevention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Cilostazol

A

phosphodiesterase inhibitor

Used for intermittent claudication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Blockers of platelet GP IIb/IIIa receptors

A

Abciximab
eptifibatide
tirofiban

Adjuncts to PCI for prevention of cardiac ischemic
complications

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

indirect thrombin and factor X inhibitors

A

unfractionated heparin
enoxaparin (low molecular weight)
fondaparinux

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

MOA of heparin

A

Antithrombin III inhibits clotting factor proteases: thrombin, IXa and Xa

Binding of heparin to antithrombin III accelerates
the inhibition.

Heparin functions as a cofactor for the antithrombin-protease reaction

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

UFH MOA

A

UFH efficiently inactivates both thrombin and
factor Xa

Ternary complex accelerates inactivation of IIa by ATIII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

LMWH MOA

A

efficiently inhibit Xa but have less
effect on thrombin

Ternary complex cannot be formed

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

what are the uses of heparins

A
  • DVT
  • Pulmonary embolism
  • MI
  • DOC during pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

AE of heparin

A

bleeding (can give protamine sulfate)

hypersensitivity

Heparin-induced Thrombocytopenia (HIT)

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

Heparin-induced Thrombocytopenia type II

A

• Antibodies recognize complexes of heparin and a
platelet protein, Platelet Factor 4.
• This leads to platelet aggregation and release of
platelet contents

IgG binds to the PF4/heparin complex forming immune
complexes
IgG binds to Fc = aggregation

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

Fondaparinux

A

Specific inhibitor of Xa.
Negligible antithrombin activity.
Approved for prevention and treatment of DVT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

MOA of warfarin

A

Warfarin antagonizes the cofactor function of
vitamin K.

Warfarin inhibits vitamin K epoxide reductase.

Treatment with warfarin results in the production
of inactive clotting factors, because they lack the
gamma - carboxyglutamyl side chains

reversal - give Vit K

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

uses of warfarin

A

Prevention and treatment of DVT and PE, following an initial course of heparin.

Prevention and treatment of thromboembolic
complications associated with AF

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

AE of warfarin

A

hemorrhage

drug induced skin necrosis (deficiency in proteins C or S)

cannot use in pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

direct thrombin inhibitor (paraenteral)

A

Desirudin
Bivalirudin
argatroban

Used in patients undergoing PCI
parenteral

22
Q

oral DTI’s

A

Dabigatran
etexilate

  • Used for prevention of stroke in patients with nonvalvular atrial fibrillation.
  • Used for prevention and treatment of DVT and PE
23
Q

direct inhibtor of Xa

A

APIXABAN & RIVAROXABAN

  • Used for prevention of stroke in patients with nonvalvular atrial fibrillation.
  • Used for prevention and treatment of DVT and PE.
24
Q

thrombolytics or firbinolytics

A

Thrombolytic drugs lyse blood clots and restore
the patency of obstructed vessels before distal
tissue necrosis occurs.

Thrombolytic agents act by converting
plasminogen to plasmin

25
Q

Alteplase

A

recombinant of tissue plasminogen factor

used for acute stroke
acute STEMI
acute pulmonary embolism

26
Q

Reteplase and tenecteplase

A

TPF recombinant with longer half life

used for acute STEMI

27
Q

plasminogen activation inhibitors

A

AMINOCAPROIC ACID & TRANEXAMIC ACID

Inhibits plasminogen activation.
Uses: adjunctive therapy in hemophilia, and
therapy for bleeding from fibrinolytic therapy.

28
Q

PROTAMINE SULFATE

A

Chemical antagonist of heparin

high in arginine

29
Q

Acute tubular injury

A

Can be ischemic or toxic

usually in the form of necrosis of tubular epithelial cells

30
Q

Inflammation (Tubulointerstitial nephritis)

A
  • Absence of nephritic or nephrotic syndrome
  • Presence of defects in tubular function

impaired ability to concentrate urine
salt wasting
metabolic acidosis

31
Q

path of ischemia of the renal tubules

A

ischemia = epithelial dysfunction = vasoconstriction = reduced GFR and oliguria

32
Q

patho of toxic damage to the renal tubules

A

toxic damage can be reversible or irreversible

reversible = loss of polarity and detachment

irreversible = necrosis and apoptosis

33
Q

parts of the nephron that are most affected by ischemia

A

tubular necrosis patchy; relatively short lengths of tubules affected, and proximal straight tubule (PST) segments and ascending limbs of Henle’s loop (HL) most vulnerable

34
Q

part of the nephron that are most affected by toxic type

A

extensive necrosis along the proximal convoluted tubule (PCT) segments with many toxins (e.g., mercury), ALSO necrosis of the distal tubule, particularly ascending HL, also occurs

35
Q

Drug induced interstitial nephritis

A

inflammatory injuries of the tubules and interstitium that are often insidious in onset and are principally manifest by azotemia

first seen in sulfonamides 
Synthetic penicillins like methicillin, ampicillin
Rifampin
Diuretics like thiazides
NSAIDs
36
Q

Acute pyelonephritis

A

Inflammation affecting the tubules, interstitium, and renal pelvis

  • Bacterial infections
  • Associated with urinary tract infections
37
Q

Chronic pyelonephritis

A

Inflammation affecting the tubules, interstitium, and renal pelvis

  • Bacterial infections
  • Associated with vesicoureteric reflux, obstruction
  • Repeated infections
38
Q

Drug Induced Interstitial Nephritis CF

A

begins 2 to 40 days after drug exposure

features:
• Fever, eosinophilia (which may be transient), rash in about 25% of patients
• Renal abnormalities- hematuria, mild proteinuria, and leukocyturia (often including eosinophils)
• 50% cases: rising creatinine or acute kidney injury with oliguria

patho:
• Drugs function as haptens and covalently bind to some plasma membrane or extracellular component of tubular cells
• These modified self antigens then become immunogenic
• The resultant injury is due to IgE or cell-mediated immune reactions directed against the tubular cells or their basement membranes

39
Q

labs of Drug Induced Interstitial Nephritis

A 
urine: 
• Eosinophils
• Sterile pyuria
• WBC casts
• Proteinuria (mild)

blood:
• Increased BUN AND creatinine
• Increased eosinophil count
• Tubular dysfunction: High K, low HCO3

histo:
• Interstitium shows variable but frequently pronounced edema and infiltration by mononuclear cells, principally lymphocytes and macrophages
• Eosinophils and neutrophils may be present often in clusters and large numbers
• Smaller numbers of plasma cells and mast cells are sometimes also present

40
Q

Pyelonephritis- Pathogenesis

A

Escherichia coli, followed by Proteus, Klebsiella, and
Enterobacter are most common

Streptococcus faecalis, also of enteric origin, staphylococci, and virtually every other bacterial and fungal agent can also cause lower urinary tract and
renal infection

In immunocompromised persons, particularly those with transplanted organs: polyomavirus, cytomegalovirus, and adenovirus

41
Q

ascending infection (pyelonephritis)

A

urethra… bladder….. kidney

From the urethra to the bladder, organisms gain entrance during urethral catheterization or other instrumentation. Long-term catheterization, in particular, carries a risk of infection

42
Q

Acute Pyelonephritis

A

Suppurative inflammation of the kidney
caused by bacterial and sometimes viral infection, which can reach the kidney by hematogenous spread or, more commonly, through the ureters in association with vesicoureteral reflux

gross:
Discrete, yellowish, raised abscesses are grossly apparent on the renal surface

histo: 
• Patchy interstitial suppurative inflammation
• Intratubular aggregates of neutrophils
• Neutrophilic tubulitis
• Tubular injury
43
Q

CF of acute pyelonephritis

A

Usually presents with a sudden onset of pain at the costovertebral angle and systemic evidence of infection, such as fever, nausea, vomiting and malaise

Along with indications of bladder and urethral irritation, such as dysuria, frequency, and urgency

lab:
• Pyuria: urine contains many leukocytes derived from the inflammatory infiltrate
• Bacteriuria
• Leukocyte casts: typically rich in neutrophils (pus casts), indicates renal involvement (because casts are formed only in tubules)
• Elevated BUN, creatinine

44
Q

papillary necrosis

A

complication of acute pyelonephritis

Seen mainly in diabetics, sickle cell disease and urinary tract obstruction

Ischemic and suppurative necrosis

Leukocytic response is limited to the junctions between preserved and destroyed tissue

45
Q

Pyonephrosis

A

complication of acute pyelonephritis

In case of obstruction, suppurative exudate is unable to drain and fills the renal pelvis, calyces, and ureter with pus

46
Q

Perinephric abscess

A

complication of acute pyelonephritis

extension of suppurative inflammation through the renal capsule into the perinephric tissue

47
Q

Chronic Pyelonephritis

A

complication of acute pyelonephritis

disorder in which chronic tubulointerstitial inflammation and scarring involve the calyces and pelvis; recurrent or persistent renal infections

etio:
recurrent infections superimposed on diffuse or
localized obstructive lesions like posterior urethral valves and kidney stones lead to recurrent bouts of renal inflammation and scarring
Reflux nephropathy (more common): superimposition of a UTI on congenital vesicoureteral reflux and intrarenal reflux

CF:
• Gradual onset of renal insufficiency or because signs of kidney disease are noticed on routine laboratory tests
• Loss of tubular function- in particular of concentrating ability- gives rise to polyuria and nocturia
• Development of hypertension
• Mild proteinuria or development of FSGS

48
Q

patho of chronic pyelonephritis

A

Gross: asymmetrical
• VUR – preferential scarring & calyceal dilatation at poles
• Obstructive – diffuse dilatation of calyces & scarring

histo:
• Uneven interstitial fibrosis and an inflammatory infiltrate of lymphocytes and plasma cells
Dilation or contraction of tubules, with atrophy of the epithelial lining
Many of the dilated tubules contain pink to blue, glassy-appearing casts- looks like thyroid hence this change is called “thyroidization”
Chronic inflammatory cell infiltration and fibrosis

Arteriolosclerosis may be caused by associated hypertension
Glomerulosclerosis that usually develops as a secondary process

49
Q

Obstructive Uropathy

A

• Obstructive lesions of the urinary tract increase
susceptibility to infection and to stone formation
• Unrelieved obstruction almost always leads to
permanent renal atrophy, termed hydronephrosis or obstructive uropathy

types of obstruction:
• Sudden or insidious
• Partial or complete
• Unilateral or bilateral

Caused by intrinsic lesions of the urinary tract or extrinsic lesions that compress the ureter

50
Q

hydronephrosis

A

Term used to describe dilation of the renal pelvis and calyces associated with progressive atrophy of the kidney due to obstruction to the outflow of urine

Tubular functional defects and interstitial inflammation with fibrosis

51
Q

Nephrolithiasis/Urolithiasis (renal stones)

A

Etiology: Idiopathic or specific disease
usually between 20 and 30

types:
calcium, triple/struvite, uric acid, cystine

patho:
• Increased concentration of stone constituents
• Changes in urinary pH
• Decreased urine volume
• Presence of bacteria influence the formation of calculi

CF:
• Silent if remain in the renal pelvis
• Symptomatic if stone passes into ureters:
• Renal colic: abrupt onset of flank pain radiating to the groin (intermittent), nausea, vomiting, gross or microscopic hematuria (ulceration of urothelium)
• Superimposed UTI – urinary stasis, trauma
• Hydronephrosis due to obstruction of the ureter

52
Q

treatment and prevention of Nephrolithiasis/Urolithiasis (renal stones)

A

Treatment options:
• IV antibiotics
• Urosurgical intervention

Prevention
By decreasing urinary concentration of the causative substances
• Increased fluid intake (2L/day)
• Low sodium diet → decrease urinary calcium excretion
• Alkalinisation of urine to increase solubility of uric acid

CRS (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions