Brainscape's Knowledge GenomeTM

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


See full index

Renal I > Pathology 7 > Flashcards

Pathology 7 Flashcards

1
Q

What is benign nephrosclerosis?

A

Sclerosis of renal arterioles and small arteries

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

What is benign nephrosclerosis associated with?

A

Some degree of ischemia –> This causes release of renin in response to the decrease in blood flow (HYPERTENSION)

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

What renal changes are seen in association with benign hypertension?

A

Hyaline arteriosclerosis

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

Where does hyaline deposit in benign nephrosclerosis?

A

Arterioles

-Get extravasation of plasma proteins through injured endothelial cells (also in BM)

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

With benign hypertension do you see renal insufficiency or uremia?

A

Not in uncomplicated cases

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

Which patient population has more severe blood pressure elevations that increase the risk of renal insufficiency?

A

Diabetes and African Americans

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

With benign nephrosclerosis what are the kidneys like?

A

They are atrophic

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

What 2 other diseases are seem simultaneously with benign hypertension

A
  1. Diabetes (Why we give ACEi to protect kidneys… they dilate efferent arteriole)
  2. Fibromuscular dysplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the clinical symptoms of benign nephrosclerosis?

A
  1. Mild oliguria
  2. Loss of concentrating mechanism
  3. Decrease GFR
  4. Mild degree of proteinuria is a constant finding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What usually kills patients with benign nephrosclerosis?

A

Hypertensive heart disease or cerebrovascular disease (not renal disease)

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

What is the pathogenesis associated with benign nephrosclerosis?

A

Medial and intimal thickening

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

What is seen in elderly patients (with or without HTN or diabetes) and in patients with long-standing diabetes, but most common and most severe in HTN patients?

A

Hyaline arteriolosclerosis

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

Is malignant hypertension more common than benign nephrosclerosis?

A

NO, less common

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

What 2 circumstances might malignant hypertension arise from?

A
  1. Novo (without pre-existing HTN)

2. Suddenly in patient with mild HTN (essential benign HTN)

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

What is the initial event in malignant HTN?

A

Some form of vascular damage to the kidney

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

What does vascular damage to the kidney result in?

A

Increased permability of small blood vessels to fibrinogen and other plasma proteins, endothelial injury, and platelet deposits

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

In malignant HTN what does increased permability of small blood vessels result in?

A

The appearance of fibrinoid necrosis in small arteries and arterioles and intravascular thrombosis

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

What does fibrinoid necrosis and intravascular thrombosis lead to?

A

Intimal hyperplasia of the vessels resulting in hyperplastic arteriosclerosis (MALIGNANT HTN)

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

What is the self-perpetuating cycle seen in malignant hypertension?

A

Narrowing of renal afferent arteriole (progressive ischemia) stimulates angiotensin II production with increased renin secretion (aldosterone will increase too)
-Constriction (angiotensin II) –> Vasoconstriction –> Ischemia –> Renin

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

What symptoms are seen with malignant HTN?

A
  1. Diastolic pressure over 130mmHg
  2. Papilledema
  3. Encephalopathy
  4. CV disorders
  5. Renal failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the early symptoms due to in malignant hypertension and what are these symptoms?

A

Increased ICP - Headache, N/V, visual

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

What is hypertensive crisis?

A
  1. Loss of consciousness, convulsions

2. Proteinuria and hematuria (90%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the frequent cause of death in malignant hypertension?

A

Uremia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What % of deaths from malignant HTN are due to CV or cerebral disorders (hemorrhage)?

A

10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe the arteriolar wall in malignant HTN

A
  • Has hyperplastic arteriolosclerosis
  • Wall is thick, narrowed lumen
  • Concentric circles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

True or False: Unilateral renal artery stenosis is an uncommon cause of HTN

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is renal artery stenosis commonly caused by?

A

Atheromatous plaque at the origin of the renal artery (70%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the second leading cause of renal artery stenosis?

A

Fibromuscular dysplasia of the renal artery (hyperplasia of all the layers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Which patient populations more frequently get renal artery stenosis due to fibromuscular dysplasia of the renal artery?

A
  1. Women

2. Younger (20-30)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Is renal artery stenosis cause a curable form of HTN?

A

Yes… it is related to the degree of stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the cause of HTN in renal stenosis?

A

Renin secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What can be used to decrease HTN due to renal stenosis?

A

ACE Inhibitors… they show marked decrease in arterial BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is seen in the kidney suffering from renal artery stenosis?

A

That kidney is ischemic and shows signs of diffuse ischemic atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

In patients with renal artery stenosis, what does their presentation minic?

A

Essential HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What technique is required to localize the stenotic lesion?

A

Ateriography

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the cure rate for renal artery stenosis?

A

70-80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What type of emboli can be seen in renal artery stenosis?

A

Cholesterol emboli (causes platelet aggregation and occasional mononuclear cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is thrombotic microangiopathies?

A

Widespread thrombosis in microcirculation causing damage to endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What 2 diseases are associated with thrombotic microangiopathies?

A
  1. Childhood hemolytic-uremia syndrome (HUS)

2. Thrombotic thrombocytopenia purpura

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is one of the main causes of acute renal failure in children?

A

Childhood hemolytic-uremia syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is seen in the vessels in thrombotic microangiopathies

A

They vasoconstrict

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What mediates vasoconstriction seen in thrombotic microangiopathies?

A
  1. Decrease NO
  2. Increased endothelin-1
  3. Decreased PGI2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is characteristically seen in microangiopathic disorders?

A

Platelet-fibrin thrombi in the glomerular capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the 2 predominant factors seen in thrombotic microangiopathies?

A
  1. Endothelial injury and activation, leading to vascular thrombosis
  2. Platelet aggregation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What does endothelial injury lead to?

A

Exposes the subendothelium which leads to decreased NO and PGI2, enhances platelet adhesion, aggregation and vasoconstriction

46
Q

What also helps to cause vasoconstriction after endothelial injury?

A

Endothelial derived endothelin-1

47
Q

What do endothelial cells secrete to cause platelet adhesion?

A

von Willebrand factor

48
Q

What normally cleaves vW factor?

A

ADAMTS-13 (vW factor-cleaving metalloprotease)

49
Q

What causes platelet aggregation?

A

vW factor secreted by endothelial cells

50
Q

What % of clinical childhood HUS follows infection?

A

75%

51
Q

What is commonly seen in clinical childhood HUS?

A

Bloody diarrhea due to intestinal infection

52
Q

What causes bloody diarrhea seen in clinical childhood HUS?

A

Verocytotoxin-releasing bacteria due to strains of E. Coli (0157:H7) which is similar to shigella toxin and activates endothelial injury

53
Q

Where can you get O157:H7 to cause clinical childhoos HUS?

A

Undercooked ground meat and petting zoos

54
Q

What are the clinical characteristics of clinical childhood HUS?

A
  1. Sudden onset (post GI or influenza infection)
  2. Hematemesis
  3. Melena
  4. Severe oliguria
  5. Hematuria
  6. Hemolytic anemia (microangiopathic)
  7. HTN in more than 50% of cases
55
Q

What is the pathogenesis of clinical childhood HUS from?

A

Shigella toxin

56
Q

What does shigella toxin affect?

A

Endothelium

57
Q

What changes are seen in the endothelium after infection by shigella toxin?

A
  1. Increased adhesion of leukocytes
  2. Increased endothelin and decreased NO
  3. Endothelial lysis (in presence of cytokines such as TNF)
58
Q

What do the changes in the endothelium favor in clinical childhood HUS?

A

Thrombosis and vasoconstriction

59
Q

What toxin can directly bind to platelets and cause activation?

A

Veryocytotoxin

60
Q

Do most patients recover from clinical childhood HUS?

A

Yes (with proper care…dialysis)

61
Q

What is the lethality in childhood HUS?

A

5%

62
Q

What is atypical/adult HUS associated with?

A
  1. Infection
  2. Antiphospholipid syndrome
  3. Pregnancy (postpartum renal failure)
  4. Vascular renal disease
  5. Chemo and immunosuppressive drugs
63
Q

What infections are associated with atypical HUS?

A
  1. Typhoid fever
  2. E. Coli Septicemia
  3. Etx or shiga toxin
  4. Viral infections
64
Q

What is the antiphospholipid syndrome associated with atypical HUS?

A

SLE (similar to membranoproliferative GN, but without immune complex deposits)

65
Q

What vascular renal diseases are assocaited with atypical HUS?

A
  1. Systemic sclerosis

2. Malignant HTN

66
Q

What drugs are associated with atypical HUS?

A
  1. Mitomycin
  2. Cyclosporin
  3. Bleomycin
  4. Cisplatin
  5. Radiation
67
Q

Inherited deficit of what causes atypical HUS?

A

Complement regulatory protein (factor H)

68
Q

Does ADAMTS13 deficiency cause atypical HUS?

A

NO

69
Q

What are the manifestations of thrombotic thrombocytopenic purpura?

A
  1. Thrombi in glomeruli
  2. Fever
  3. Hemolytic anemia
  4. Neurologic symptoms
  5. Thrombocytopenic purpura
70
Q

What defect, whether inherited or acquired, causes thrombotic thrombocytopenic purpura?

A

ADAMTS-13

71
Q

What does ADAMTS-13 normally do?

A

-Normally cleaves large vW multimer (large vW factors promote platelet adhesion and aggregation)

72
Q

Is thrombotic thrombocytopenic purpurea more common in women or men, older or younger

A

Most patients are women under 40

73
Q

What is the dominant feature of thrombotic thrombocytopenic purpura?

A

Neurologic involement

74
Q

What % of patients with thrombotic thrombocytopenic purpura experience renal involvement?

A

50%

75
Q

What is the renal involvement seen in thrombotic thrombocytopenic purpura?

A
  1. Eosinophilic thrombi in glomerular capillaries, interlobular artery, and afferent arterioles (similar changes as with HUS)
76
Q

What is the treatment of thrombotic thrombocytopenic purpura?

A

Exchange transfusion and steroid treatment (this lowers the mortality rate to below 50%

77
Q

What does increased exposure of vWF to ADAMTS-13 cause?

A

A predisposition to bleeding by causing increased degradation of vWF (characterized by one type of von Willebrand disease)

78
Q

What are 2 manifestations of disease characterized by a combination of thrombocytopenia and microangiopathic hemolytic anemia?

A
  1. Thrombotic thrombocytopenic purpura

2. Hemolytic uremic syndrome

79
Q

What are the 3 main steps in pathogenesis of TTP and HUS?

A
  1. Start with activation and intravascular agglutination of platelets (micro thrombi)
  2. Micro thrombi can cause ischemia of multiple organs (brain and kidney)
  3. Induce mechanical damage to RBCs resulting in intravascular hemolysis
80
Q

What causes platelet activation in HUS?

A

Damage to endothelial cells by Shiga toxin-producing bacteria (E. Coli O157:H7)

81
Q

What causes platelet activation in TTP?

A

The binding of abnormally large multimers fo vWF to platelets

82
Q

What can cause large forms of vWF?

A

A deficit in ADAMTS-13 (which causes cleavage of large vWF multimers

83
Q

What are the clinical maifestations of TTP and HUS?

A
  1. Thrombocytopenia
  2. Hemolytic anemia
  3. Renal failure (more pronounced in HUS)
  4. Fever
  5. Mental status changes
84
Q

What lab abnormalities are seen in TTP and HUS?

A
  1. Thrombocytopenia
  2. Evidence of hemolysis (increased bilirubin, LDH, low haptoglobin, high retic count)
  3. Anemia with the presence of schistocytes
85
Q

Are PT and PTT normal in TTP and HUS?

A

Yes

86
Q

Do children with HUS get better with supportive care?

A

Yes

87
Q

What are patients with TTP treated with?

A

Plasma Exchange

88
Q

What is immune thrombocytopenic purpura?

A

Development of auto-immune antibodies (not activating) against platelet surface antigens, IgG

89
Q

How do you diagnose immune thrombocytopenic purpura?

A

This is a diagnosis of exclusion

-No specific diagnostic study defines ITP, only made by excluding other causes of thrombocytopenia

90
Q

What is seen clinically in immune thrombocytopenic purpura?

A

Moderate to severe thrombocytopenia without any other laboratory abnormalities

91
Q

What is seen in bone marro for immune thrombocytopenic purpura?

A

Reactive megakaryocytic hyperplasia

92
Q

What is the treatment for children with immune thrombocytopenic purpura?

A

Usually have spontaneous resolution (treatment is supportive)

93
Q

When are platelet transfusions used in immune thrombocytopenic purpura

A

Only for life threatening bleeding

94
Q

What do you use to treat adults with immune thrombocytopenic purpura?

A

Immune modulating drugs or splenectomy

95
Q

In adults that have chronic recurrent ITP what is treatment aimed at?

A

Preventing major bleeding rather than cure of ITP

96
Q

What drugs can be given for immune thrombocytopenic purpura?

A
  1. Prednisone
  2. Dexamethasone
  3. IVIG
97
Q

Who do you see atherosclerotic rental disease causing bilateral stenosis in?

A

Older adults

98
Q

What does atherosclerotic renal disease causing bilateral stenosis cause?

A

Chronic ischemia

99
Q

What results from atheroma in older patients with severe atherosclerosis?

A

Atheroembolic renal disease

100
Q

What happens in sickle cell disease?

A

The vasa recta gets plugged by sickled cells

101
Q

What results from the vasa recta being plugged by sickle cells?

A
  1. Hematuria
  2. Decrease renal concentrating mechanism
  3. Patchy papillary necrosis
  4. Proteinuria
102
Q

When do you see diffuse cortical necrosis?

A
  1. Following obstetric emergency
  2. Septic shock
  3. Following extensive surgery
103
Q

What is seen in diffuse cortical necrosis?

A

Glomerular and arteriolar microthrombi

104
Q

Is diffuse cortical necrosis compatible with survival?

A

Yes, the unilateral or patchy involvement is compatible with survival

105
Q

What are the favored sites for infarcts?

A

End organ nature of vasculature

106
Q

What are most infarct due to?

A

Emboli via left venticle/artia as a result of MI

-This is a mural thrombosis

107
Q

What’s a good stain for hylaine?

A

Conga Red

108
Q

What does hyaline arteriolosclerosis cause?

A

Patchy ischemic atrophy with focal loss of parenchyma that gives the surface of the kidney the characteristic granular appearance

109
Q

What is renal artery stenosis?

A

A narrowing or blockage of the renal arery, which supplies blood to the kidneys

110
Q

What can significant renal artery stenosis contribute to?

A

HTN (high blood pressure) and can be a factor in renal failure

111
Q

What is the second most common type of renal artery stenosis?

A

Fibromuscular dysplasia

Renal I (8 decks)

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