Brainscape's Knowledge GenomeTM

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


See full index

Path 1 > Path 2 first quiz > Flashcards

Path 2 first quiz Flashcards

1
Q

functions of the kidney

A

Blood pH
water and salt concentration
waste elimination
hormones

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

hormones of the kidney

A

Renin-BP
erythropoeitin
prostaglandings

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

prostaglandins

A

precursors for hormones

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

forms RBCs

A

erythropoietin

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

four compartments

A

glomeruli-filtration of blood:Renin-BP
tubules-collection system
Interstitial tissues
Vessels of the kidney

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

glomular pathology

A

usually immunological

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

pathology of the tubules

A

due to bacterial toxins

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

pseudo fenstration

A

holes in endothelial tissue that filter blood

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

between 2 _____ are filtration slits and they are important for the formation of _____

A

podocyte, urine

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

Mesangial cells are a type of _____ cell that occupies space within the ______

A

stromal, glomeruli

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

this cell can replicate, fight infection, and become sclerotic if there is excess proliferation

A

mesangial cells

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

antibody-antigen complex attaches to the wall of vessels. deposited between basement membrane and endothelial cells

A

circulating immune complex deposition

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

subentimal layer

A

between basement membrane and endothelial cells

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

circulating immune complex deposition is a type ___ hypersensitivity

A

III

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

prevents normal filtration of the blood due to

A

circulating immune complex deposition

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

Heymann’s glomerular nephritis is not a _____ reaction

A

hypersensitivity

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

Anti-GBM glomerulonephritis

A

Type 2 hypersensitivity-destroys podocytes

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

are very permeable to water, but impermeable to blood cells, proteins, albumins

A

Glomeruli

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

for unknown reasons, the glomeruli is damaged and there is increased
permeability of RBC’s and decreased permeability of water.

A

In nephritic syndrome

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

blood in the urine, with red blood casts

A

Hematuria

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

(limited or diminished amount of urine produced)

A

Oliguria

22
Q

production of renin is the first step in a cascade. The end product is the formation of Angiotensin
II, which leads to the____ in the blood pressure.

A

increase

23
Q

elevated blood levels of
blood urea nitrogen AKA: BUN and creatinine which is closely related to reduced glomerular
filtration rate

A

azotemia

24
Q

antibodies of streptococcus is produced and the antibodies can also
destroy the glomerular wall

A

Acute Proliferative Glomerulonephritis

25
Q

Some viral infections (measles, etc) in children may also result in this condition. It is curable
with corticosteroids

A

Acute Proliferative Glomerulonephritis

26
Q

50% of cases of this in the adult is transferred

into chronic glomerularnephritis and only 1% in children

A

Acute Proliferative Glomerulonephritis

27
Q

swelling underneath the eyes – common with

A

kidney problem

28
Q

MOST DANGEROUS. it is a complex of
disorders (not a disease) characterized by rapid and progressive kidney pathology (oligouria) and
death within weeks or months.

A

Rapidly Progressive (Crescentic) Glomerulonephritis

29
Q

glomeruli will become crescent shaped and obstruct the lumen of the proximal convoluted
tubule and urine will build up inside the kidney and increase hydrostatic pressure within the
glomerular basement membrane. This prevents circulation of the blood. (the prognosis of the
disease is based in the amount of crescent cells – 80% or more is fatal)

A

Rapidly Progressive (Crescentic) Glomerulonephritis

30
Q

idiopathic more than 50%

A

Type I- (Anti-GBM)- ( type II

hypersensitivity reaction)

31
Q

characterized by development of
autoimmune aggression against two basement membranes. The Abs will form against
Ags of the membranes. (lungs and kidney)

A

Good pasture’s syndrome (anti-GCM)

32
Q

This is curable, via plasmapheresis

A

Good pasture’s syndrome

33
Q

if there is protein in the urine =

A

PATHOLOGY

34
Q

development of aggression against the basement membrane ( type II
hypersensitivity reaction)

A

Type I- (Anti-GBM)

35
Q

it is associated with Type III hypersensitivity

reactions.

A

Type II- (Immune Complex Deposition)

36
Q

Systemic lupus erythematosus is associated with

A

Type II- (Immune Complex Deposition)

37
Q

classic autoimmune disease that involves young ladies

– 20s. It is more common in African Americans

A

Systemic lupus erythematosus

38
Q

Causes – UV radiation, intake of

sulfasalysitic drugs, vaccination

A

Systemic lupus erythematosus

39
Q

It mostly involves the skin, lungs, kidney
and cerebral vessels. Results in serious hypertension and possibly stroke. Primary
manifestation of systemic lupus is the butterfly rash. Lupus Nephritis – involvement of
the kidneys, develops quickly. This is the major cause of death in this disease. Vasculitis
of cerebral vessels is possible in SLE

A

Systemic lupus erythematosus

40
Q

● survival is 90% at the present time

● TMT – corticosteroid therapy

A

Systemic lupus erythematosus

41
Q

characterized by the development of vasculitis. It is inflammation of
the vascular wall. MOST DANGEROUS. Manifested by anti-neutrophil plasmocytic
auto-antibodies. This tells us there is an autoimmune disorder that results in vasculitis.

A

Type III - (Pauci-immune)

42
Q

develops in middle aged males (can be women in older
age). It is characterized by necrotizing vasculitis of the upper and lower respiratory tract
and rapidly progressing of glomerulonephritis (kidneys). You see a melting of the bones
of the face which can lead to infection and supperative inflammation. The patient is
undergoing decay. Patient will die due to acute renal failure, or secondary
complications.

A

Wegener’s Granulematosus

43
Q

characterized by vasculitis of the vessels throughout the body (middle and small sized arteries). With the pouching of the arteriole wall,
which gives it the name nodosa. Because of the inflammation causes weakness of the wall and pouching. The pouching of the walls can lead to rupture of the wall and obstruction of the lumen. These nodes are on every organ of the body and causes death. This disease can manifest in any organ except the lungs and the arch of the
aorta . INCURABLE. NETTER PICTURE

A

Polyarteritis (Periarteritis) Nodosa

44
Q

Hematuria following an acute respiratory infection. Many cases month after month. Could also be caused by an acute intestinal or urinary infection. The patient will experience pain in the loin (lumbar spine). One of the most common diseases associated with gross hematuria. MOST COMMON glomerular disease worldwide. Hallmark is the deposition of IgA immune complexes into the
immune mesagium. (50% increase in IgA). There will also be increased concentration of IgA in the blood and IgA immune complexes in the blood. Can manifest with Henoch-Schonlein Purpura. If not controlled can switch to chronic glomerulonephritis.

A

IgA Nephropathy (Berger’s Disease)

45
Q

Type III - (Pauci-immune)

A 
Wegener's Granulematosus
Polyarteritis (Periarteritis) Nodosa
IgA Nephropathy (Berger’s Disease)
46
Q

Henoch-Schonlein Purpura (hemorrhagic vasculitis)- usually develops in boys in their 20’s. It is characterized by four clinical syndromes:

A

abdominal syndrome
cutaneous syndrome
articular syndrome
crescentic glomerulonephritis

47
Q

abdominal syndrome

A

it is characterized by hemorrhagic inflammation of

the stomach and duodedenal walls (gastroduodenitis).

48
Q

cutaneous syndrome

A

subcutaneous hemorrhages in the buttock and

abdomen – leads to the development of purpura rash

49
Q

articular syndrome

A

characterized by subclinical arthritis or at least pain

in the joints.

50
Q

crescentic glomerulonephritis

A

if the patient has the first three
syndromes - and if you add crescatic glomerular nephritis makes the
prognosis much worse – 70%.

Path 1 (14 decks)

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