Brainscape's Knowledge GenomeTM

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


See full index

Module 3.5 > Path > Flashcards

Path Flashcards

1
Q

Give a quick breakdown of sarcoid

A

**Disease **

Forms Noncaseating granulomas in many tissues - hilar lymphadonopathy, lung eye and skin

Etiology and Pathogenesis

Unknown, probaby immune regulation failure after exposure to environmental agent

T-cells accumulate and give off cytokines such as IL-2, INF-y, TNF (so high in lungs it is diagnostic)

**Morphology **

Noncaseating granulomas (schaumann and asteroid bodies like TB)

Lungs, Lymph, Spleen, Skin lesions

Course

Insideous onset respiratory abnormalities including hemoptysis,

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

Describe asbestos related diseases

A

Dieases

Fibrous plaques, or diffuse pleural fibrosis

Pleural effusions

Parenchymal interstital fibrosis

Lung Carcinoma

Mesothelioma

Some lung neoplasms

**Pathogenesis **

Serpentine and amphibole fibers, the latter being worse

Exacerbates carcinogenic effect of smoking

Prussian blue to stain ferruginus bodies

Clinical Course

Dyspnea, productive cough, lower lobe density. Asbestosis with other cancers is lethal.

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

Conjunctivitis

A

H. Influenzae

Adenovirus

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

Otitis media

A

H. Influenzae

Strep pneumonia

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

Otitis externa

A

Pseudomonas

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

Pharyngitis

A

Group A strep Diphtheria (pseudo membrane) stops protein synthesis by affecting ADP

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

Epiglottis

A

H. Influenzae

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

Endocarditis

A

Staph A,

Staph

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

Common cold

A

Rhinovirus

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

Influenza

A

Enveloped negative sense RNA capable of genetic drift

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

Community acquired URI with conjunctivitis

A

Adenovirus Big in the military, can cause serious infection and death

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

Mono

A

Epstein Barr DNA virus,

replicates is respiratory b-cells and specifically in their nucleus

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

Acute “typical” pneumonia

A

Strep Pneumoniae (1)

Staph Aureus (2)

Klebsiella

Pseudemonas (burn victims)

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

Atypical pneumonia

A

Chlamydia pneumonphila

Mycoplasma pneumonia

Mycobacterium

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

Older folks

A

Mycoses

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

Ohio river

A

Histomycoses

17
Q

Mississippi, south Easter us

A

Blastoplasmycoses

18
Q

San Joaquin valley

A

Coccidiomycosis

19
Q

Renal Cell carcinoma

A

Diagnostic Features

Costovertebral pain, Palpable mass, Hematuria

Risk factors

60+, Men, Smoking 2:1

Large mass in one pole of kidney

Orange color, hemorrhage, necrosis and cystic change

Common metastasis, Lung>Bone>Lymph

Can invade vein and form a floating line to the heart.

20
Q

Clear Cell Carcinoma

A

The most common Renal Cell Carcinoma

98% sgiw sgirt arm Chromasom 3 deletion

Gene deletion prevents normal breakdown of protein leading to angiogenic factors like VEGF, PDGF, TGFa

21
Q

Papillary Carcinoma

A

Frequently multifocal

associated with trisomies 7, 16, 17 and loss of Y

composed of low columnar cells arranged in papillary formations

22
Q

Cystic Diseases of the kidney

A

Most common are

Auto Dominant

Auto Recessive

23
Q

Auto Dominant PKD

A

1~600 live births

renal function retained till 50

mutation of PDK1 gene worse than PDK2

PDK2 associated with Ca2+ channels

Kidneys can be 4kg, grossly distended

Clinical Features

Hematuria, proteinuria, “Dragging sensation”.

At risk

Blacks, men, hypertensive

Additional Concerns

Liver cyst, berry aneurysms, Mitral valve prolapse

24
Q

Auto Recessive PKD

A

Primary gene abnormality is PKHD1 - fibrocystin (function unknown)

External appeance is normal, cysts are internal, cuboidal lined derived from collecting ducts.

Major concern is associated Liver Fibrosis

25
Obstructive Uropathy
May remain silent for long periods, If quickly resolved condition is reversable leads to period of diuria Congenital anomalies urinary calculi prostatic hypertrophy Tumors inflammation blood clots pregnancy uterine prolapse
26
Acute Kidney Injury
Patterns are ischemic and nephrotoxic Three phases, Initiation, maintenance, recovery Eosinophilic Hyaline Casts and pigmented granular casts in the damaged nephrons "tamm-Horsfall protein" Flattened epithelial cells with hyperchormatic nuclei and mitotic figures are often present leading to full repair (NOT CANCER) "Proper management means the difference between full recovery and death." Damage in the tububles causes protein movement, including redistribution of the Na/K pump to the luminal wall, pumping Na out and causing "tubuloglomerular feedback" TGFa critical in repair
27
Nephritic syndrome
Acute onset of visible hematuria, proteinuria, hypertension. Classic presention of Acute Poststreptococcal Glomerulonephritis. Enlarged hypercellular glomeruli, diffuse in all lobes. Immnunofluorescense shows IgG, IgM and C3 along the basement membrane in HUMPS
28
Nephrotic syndrome
Heavy proteinuria \> 3.5 gm/day Hypoalbuminemia Severe edema Hyperlipidemia lipiduria loss of anticoagulant factors can lead to thrombotic prolems In kids neohrotic syndrom = lesion in adults usually systemic disease.(diabetes, amyloidosis and SLE Include Minimal Change disease, membranous glomerulopathy, FSGS
29
Poststrep Glomerular nerphitis
All glomeruli are enlarged and hyper cellular diffuse leukocyte and neutrophil inflitration RBC casts in tubes and urine immunofluorescence shows IgG, IgM and C3 in focal deposits. EM shows dense "humps" Classic, young child 1 week after strep presents with nephretic symptoms, Labs: low complement and high antistrep titers
30
Rapidly Progressive Glomerular Nephritis
Crescents in glomeruli from proliferating epithelium Type 1 Anti Gbasement membrane Include GoodPasture syndrom (linear IgG and pulmonary hemorrhages. Need to supress antibodies) Type 2 Immune complex depostion follows other immune complex problems. Usually has cellular proliferation in the glomeruli and cresents. Ig deposition pattern is granular. Type 3. pauci-immune type no anti GBM antibodies, but antineutrophil cytoplasmic antibodies. Can be a component of Wegeners, Mostly idiopathic. viewed as a vasculitic disease. Morphology Kidneys enlarged and pale, possible focal necrosis. Crescents.
31
Membranous Nephropathy
diffuse thickening of glamerular capillary wall, accumlation of Ig containing deposits along the subepithelial side of the basement membrane. "Spike and dome, hair on end" capillary loops
32
## Footnote cystitis
## Footnote introduction of vaginal or bowel bacteria to the urethra... Symptoms: dysuria, frequent urination, supra public pain. Unidirectional flow, low pH, urea, organic acids, lactofrrin are protectitive. Women more at risk, sexual intercourse
33
## Footnote pyelonephritis
## Footnote flank pain, nausea vomiting and chills, .
34
## Footnote uncomplicated uti
## Footnote ecoli, gram negative anaerobes
35
## Footnote complicated UTI
## Footnote associated with damage that prevents renal flow... Fevers, leukocytosis, pyuria ... E.coli... Proteus, mirabilis... Pseudomonas aeurginosa... Staph aureus.. Staph epi...

Module 3.5 (7 decks)

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