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Boards - Step 1 > Pathoma Ch 9, 12 (Resp Tract, Renal/Urinary Tract) > Flashcards

Pathoma Ch 9, 12 (Resp Tract, Renal/Urinary Tract) Flashcards

-Resp Tract (ch9) -(ch19)

1
Q

MC cause of

(a) rhinitis
(b) acute epiglottitis
(c) laryngotracheobronchitis

A

MC cause

(a) Rhinitis = adenovirus
(b) Acute epiglottitis = H. influenza B
- MC cause in BOTH vaccinated and unvaccinated
(c) laryngotracheobronchitis = croup = parainfluenza

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2
Q

What type of hypersensitivity is allergic rhinitis?

A

Type I hypersensitivity- preformed antibodies to pollen

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3
Q

List three causes of nasal polyps

A
  1. Recurrent rhinitis
  2. CF
  3. Aspirin-induced asthma
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4
Q

Triad of aspirin-induced asthma

A

Aspirin-induced asthma is seen in 10% of adult asthmatics

  1. Asthma
  2. Aspirin induced bronchospasm
  3. Nasal polyps
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5
Q

Demographic for angiofibroma of the nasopharynx

(a) Clinical presentation

A

Angiofibroma = benign tumor of BV, in young adult males

(a) Epistaxis

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6
Q

2 populations who you see nasopharyngeal carcinoma in

(a) Typical clinical feature

A

Nasopharyngeal carcinoma (associated w/ EBV) in African children and Chinese adults

(a) Cervical lymphadenopathy

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7
Q

Histologic findings of nasopharyngeal carcinoma

A

Key is keratin-positive cells- recall keratin is the intermediate filament of epithelial cells => keratin-positive proves its epithelium => carcinoma

Pleomorphic keratin-positive ep cells in background of lymphocytes

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8
Q

Explain physiology of vocal cord nodules

(a) Composition
(b) Clinical presentation
(c) Tx

A

Vocal cord nodules (‘nodesss!!! #pitchperfect) = nodule on the true vocal cords

(a) Myxoid (degenerative) CT from overuse
(b) Presents w/ hoarseness
(c) Voice rest

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9
Q

Laryngeal papilloma

(a) Etiology
(b) Adults vs. children

A

Laryngeal papilloma = finger-like projection on the larynx

(a) HPV serotypes 6 and 11 (low-risk)
- HPV => see koilocytic changes on histology
(b) Single in adults but multiple in children

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10
Q

2 RF for laryngeal carcinoma

A

Smoking and EtOH- same as for nasopharyngeal, basically squamous cell carcinomas due to exposure to smoking and EtOH in respiratory tracts

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11
Q

Explain how URI predisposes pt to superimposed bacterial pneumonia

(a) MC bacteria

A

Virus can impair the airway lining (cilia) => disrupt the mucociliary elevator used to clear stuff from airways

So decreased defenses => increased risk of bacterial superinfection

(a) Secondary pneumonia MC cause
1. strep pneumo (lobar)
2nd is staph aureus (bronchopneumonia)

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12
Q

2 main molecular mediators of pain

A

Bradykinin and PGE2 (prostaglandin E2)

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13
Q

MC cause of

(a) Lobar pneumonia
(b) Atypical pneumonia
(c) Pneumonia complicated by autoimmune hemolytic anemia

A

MC cause of

(a) Lobar pneumonia = strep pneumo
(b) Atypical pneumonia = mycoplasma pneumonia
(c) Mycoplasma pneumoniae can cause AI hemolytic anemia (IgM, cold agglutinin)

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14
Q

Which organism causes pneumonia w/ currant jelly colored sputum

A

Klebsiella pneumoniae- causes 5% of lobar pneumonias (other 95% are strep pneumo) has thick mucoid capsule causing gelatinous sputum (currant jelly)

GROSS

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15
Q

Bacterial pneumonia that is not visible on gram stain

A

Mycoplasma pneumoniae- not visible on gram stain due to lack of cell wall

MC cause of atypical (interstitial) pneumonia

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16
Q

Describe the pattern of pneumonia caused by H. influenzae and legionella pneumophila

A

Both H. influenzae and legionella pneumophila cause bronchopneumonia- scattered patchy consodliations centered around the bronchioles, often multifocal and b/l

Basically patchy and along the airways = bronchopnuemonia

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17
Q

Differentiate the pattern of involvement of bronchopneumonia and atypical pneumonia

A

Bronchopneumonia (S. aureus, H. influenza, pseudomonas, moraxella, and legionella) causes patchy infiltrates b/l along the airways

Interstitial/atypical pneumonia (mycoplasma, chlamydia, RSV, CMV, influenza, coxiella burnetii) causes infiltrate into the CT lining the alveoli (in the alveolar wall), so this causes increased pulmonary markings on CXR

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18
Q

MC bacteria involved in aspiration pneumonia

A

Anaerobic bacteria of the oropharynx

Bacteroides, Fusobacterium, Peptococcus

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19
Q

Name bacteria that you use silver stain to visualize

A

Bacteria mostly pseudomonas and legionella (both causes of bronchopneumonia)

Then also to stain fungi such as pneumocystis and candida

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20
Q

Name 2 organisms that commonly cause pneumonia superimposed on COPD

A

Pneumonia superimposed on COPD (leading to exacerbation of COPD) 2/2 H. influenzae and moraxella catarrhalis

Both of which cause bronchopneumonia (scattered patchy consolidations centered around bronchioles)

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21
Q

Young adult p/w interstitial pneumonia that is negative for mycoplasma

Next dx?

A

Chlamydia pneumoniae = 2nd MC cause of atypical pneumonia in young adults

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22
Q

MC cause of atypical pneumonia in

(a) young adults
(b) infants
(c) Posttransplant immunsuppressive therapy

A

MC cause of interstitial/atypical pneumonia in

(a) Young adults = mycoplasma
- 2nd is chlamydia pneumoniae
(b) Infants = RSV (respiratory syncytial virus)
(c) Posttransplant/immunosuppressed = CMV

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23
Q

What is Q-fever?

A

Q-fever = infxn caused by coxiella burnetti (rickettsial organism) that can cause interstitial (atypical) pneumonia

Presents w/ flu-like symptoms w/ high fever

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24
Q

Explain how elderly die if they die from the influenza virus

A

Influenza virus causes an atypical pneumonia in immunocompromised or existing disease, then this increases the risk of bacterial superinfection w/ S. aureus or H influenza

So they die from from the superimposed bacterial infection, not the influenza virus

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25
Q

MC organ involved when Tb spreads systemically

A

Kidneys, causing sterile pyuria

Sterile pyuria = elevated white count in urine w/o bacteria in urine

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26
Q

Ddx for caseating granulomas

A
  1. MTb (duh)

2. Fungi

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27
Q

Explain the physiology behind the clinical presentation of chronic bronchitis

A

Chronic bronchitis = productive cough for 3+ months over at least 2 years due to hypertrophy of the bronchial mucinous glands

-basically the mucous glands (produce mucus) hypertrophy in response to cig smoke => tons of mucus secreted

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28
Q

‘blue bloaters’ vs. ‘pink-puffers’

A

Two types of obstructive pulmonary disease

Blue-bloaters = chronic bronchitis- cyanosis b/c mucus plugs trap CO2

Pink-puffers = Emphysema- prolonged expiration w/ pursed lips, increased work of breathing

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29
Q

Explain the cause of obstruction in emphysema

A

In emphysema the obstruction is not physical as seen by mucus plugs in chronic bronchitis

Instead the loss of recoil of the interstitium decreases force at which air is pushed out, also loss of recoil of the non-cartilage containing bronchioles causes collapse of airways (air stuck behind collapsed airways)

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30
Q

Explain how alveolar air sacs are destroyed in emphysema

A

Emphysema: imbalance btwn proteases (elastase and other proteases from neutrophils called in by inflammation) and anti-proteases from chronic inflammation

Aka cig smoke increases inflammation => more neutrophils produce more proteases that overwhelm the antiproteases

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31
Q

Explain why the risk of cirrhosis is increased in alpha-1 antitrypsin

A

B/c misfolded alpha-1 antitrypsin protein accumulates in the endoplasmic reticulum of the hepatocytes

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32
Q

Differentiate clinical features of chronic bronchitis and emphysema

A

Chronic bronchitis- very productive (literally buckets of sputum) cough, cyanosis (blue bloaters)

Emphysema- non-productive cough, prolonged expiration w/ pursed lips (auto-PEEP)

Both have increased risk of hypoxemia and cor pulmonale

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33
Q

What is the FRC?

(a) How is it changed in emphysema?
(b) Change seen in pulmonary fibrosis?

A

FRC = functional reserve capacity = where the curves meet btwn chest wall pulling outwards and pulmonary recoil pulling inwards

(a) In emphysema the recoil is decreased => FRC increases
- see ‘barrel chest’/increased AP diameter on CXR

(b) Pulmonary fibrosis- FRC decreased b/c fibrosis keeps lung stiff and inwards

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34
Q

Explain development of core pulmonale 2/2 obstructive lung disease

A

Lungs vasoconstrict perfusion to areas of low ventilation, but doesn’t know that there are no good areas on ventilation in diffuse obstructive disease => diffuse vasoconstriction of pulmonary vasculature makes high resistance for right heart to push against

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35
Q

What type of hypersensitivity is asthma?

(a) Main cell type involved in initial exposure?

A

Asthma = type I hypersensitivity, pre-sensitized IgE release histamine immediately in response to exposure

(a) Initial exposure- Th2 phenotype CD4 T cells are the main cells involved

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36
Q

Give the function of the the three main interleukins released in asthma response

A

Th2 type CD4 cells secrete

  • IL-4: mediates class switch of plasma cell to IgE
  • IL-5: attracts eosinophils
  • IL-10: stimulates Th2 cells and inhibits Th1 cells, so propagates more Th2
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37
Q

Differentiate the factors that mediate the early phase and late phase reactions in asthma

A

Reexposure to allergic leads to IgE-mediated activation of mast cells

Early phase reaction = release of preformed histamine granules (vasodilation of arterioles, venule leakiness) and leukotriene release

Then late-phase reaction maintained by major basic protein from eosinophils to perpetuate the bronchoconstriction

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38
Q

Name some nonallergic causes of asthma

A
  1. exercise
  2. infection
  3. aspirin (seen w/ bronchospasm and nasal polyps
  4. occupational exposures
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39
Q

What is bronchiectasis?

(a) Obstructive or restrictive?

A

Bronchiectasis = permanent dilation of bronchioles and bronchi (distal airways)

(a) Obstructive b/c dilation causes loss of airway tone resulting in air trapping, can’t generate enough velocity to get air of larger tubes

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40
Q

Defect that causes Kartagener syndrome

A

Inherited defect of the dynein arm of cilia => primary ciliary dysmotility
-sinusitis, infertility, situs inversus

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41
Q

Name an infectious cause of bronchiectasis

A

ABPA = allergic bronchopulmonary aspergillosis = hypersensitivity rxn to Aspergillus that causes chronic inflammatory damage

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42
Q

Which subtype of obstructive pulmonary disease can cause foul-smelling sputum?

A

Bronchiectasis- dilated airways get build up behind them => mucus stays trapped (ew gross)
-CF pts, Kartagener’s

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43
Q

Pathophysiology of idiopathic pulmonary fibrosis

A

IPF: fibrosis (thickening) of the intersititum of the lungs (wall of alveoli)

-cyclic lung injury (from unknown cause, hence idiopathic) causes release of TGF-beta from injured pneumocytes, its this TGF-beta that induces fibrosis

Key here is TGF-beta => fibrosis

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44
Q

2 drugs classically implicated in secondary pulmonary fibrosis

A
  1. bleomycin

2. amiodarone

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45
Q

Tx for idiopathic pulmonary fibrosis

A

Lung transplant b/c can’t remove the fibrosis, can’t thin the alveolar walls!

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46
Q

Explain the physiology of pneumoconioses

A

Pneumoconioses = interstitial pulmonary fibrosis due to chronic environmental exposure (MC occupational) to small particles (have to be small so can get to the most distal airways) that are fibrogenic (have to stimulate alveolar macrophages to induce fibrosis)

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47
Q

Differentiate anthracosis and coal workers’ pneumoconiosis

A

Anthracosis = clinically benign mild exposure to carbon that causes collection of carbon-laden macrophages
-super common 2/2 air pollution

Far extreme form = chronic exposure to carbon dust seen in coal miners => diffuse fibrosis (‘black lung’)
-lolllllz “Paaaa I think I caught the black lung” #zoolander

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48
Q

Which pneumoconiosis increases the risk for TB infection

A

Silicosis (silica exposure, sandblasts and silica miners) impairs phagolysosome formation => increases risk of TB

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49
Q

Which pneumoconiosis pathologically looks like sarcoidosis?

A

Berylliosis (beryllium exposure in aerospace injury) causes noncaseating granulomas in lungs, hilar LN, and systemic organs (same pathology as sarcoid!)

So if question is a NASA worker than seems to have sarcoid, think about berylliosis

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50
Q

MC cancer 2/2 asbestosis exposure

A

WATCH OUT
MC is still lung carcinoma

There is an increased risk of mesothelioma, but STILL THE MC is lung carcinoma

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51
Q

Sarcoidosis

(a) Obstructive or restrictive lung disease?
(b) MC presenting symptom
(c) Classic demographic

A

Sarcoidosis

(a) Restrictive- granulomas restrict filling b/c reduce compliance of interstitium
(b) Cough
(c) African American females

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52
Q

2 lab value abnormalities in sarcoidosis

A

Sarcoidosis

  1. elevated ACE
  2. Hypercalcemia- epithelioid histiocytes contain active 1-alpha hydroxylase that activates vitamin D
    - seen in any disease w/ noncaseating granulomas (ex: Berylliosis too from beryllium exposure)
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53
Q

Name tissues besides lung that are commonly involved in Sarcoidosis

A

Uvea- uveitis
Skin- cutaneous nodules or erythema nodosum
Salivary/lacrimal glands- can mimic Sjogrens
-but almost any tissue can be involved

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54
Q

MC location of granulomas in sarcoidosis

A

Noncaseating granulomas in multiple organs, but MC involving hilar lymph nodes and then lung

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55
Q

Granulomas w/ eosinophils

(a) Dx
(b) Long term consequence

A

Granulomas w/ eosinophils (a) Hypersensitivty pneumonitis (pigeon breeder from Hey Arnold)

(b) Interstitial fibrosis after long term exposure to antigen (pigeon poop)

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56
Q

Mutation associated w/ primary pulmonary hypertension

A

Young adult females w/ inactivating mutations of BMPR2 leading to proliferation of vascular smooth muscle which thickens the pulmonary vessel walls

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57
Q

Define pulmonary hypertension

(a) Locate the atherosclerosis

A

High pressure in pulmonary circuit, defined as over 25 mmHg (while normal is 10 mmHg)

(a) Atherosclerosis of the pulmonary artery

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58
Q

Why does ARDS recover w/ interstitial fibrosis and not just regeneration as seen in mild pneumonias

A

ARDS- free radicals damage the type I and type II pneumocytes (stem cells)

When stem cells are damaged you can’t regenerate the tissue => regenerates w/ fibrosis and scar

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59
Q

2 functions of type II pneumocytes

A

Type II pneumocytes produce surfactant and are the stem cells to regenerate type I

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60
Q

Why may maternal diabetes increase risk of neonatal respiratory distress syndrome

A

Maternal insulin doesn’t cross placenta but maternal glucose crosses placenta and causes fetus to overproduce insulin, then fetal insulin inhibits surfactant production

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61
Q

How does neonatal respiratory distress syndrome increase risk of

(a) PDA
(b) necrotizing enterocolitis
(c) blindness

A

NRDS

(a) Patent ductus b/c not the right oxygen tension to close
(b) Nec b/c less O2 to the gut
(c) Blindness b/c ROS damage to the eye
- before we gave steroids to increase fetal surfactant production, NRDS was one of the leading causes of neonatal blindness

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62
Q

Main carcinogen found in cig smoke

A

Polycyclic aromatic hydrocarbons

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63
Q

2 causes of benign ‘coil lesions’ found on CXR

A

Coin lesions (esp in young pts) can be benign

  1. Granuloma- Tb or fungus (ex: histoplasma in midwest)
  2. Bronchial hamartoma = benign tumor of lung tissue and cartilage
64
Q

Small cell vs. non-small cell lung carcinoma

(a) MC
(b) Tx

A

Lung carcinoma divided into two categories

Small cell

(a) 15%
(b) ‘cells to small for surgeon to get’- tx primary w/ chemo/radiation, usually not amenable to surgical resection

Non-small cell

(a) 85% so much more common and hads bunch of subtypes: adenocarcinoma, squamous cell, large cell, carcinoid
(b) first line tx is surgical resection

65
Q

Which lung cancers are

(a) Central
(b) Peripheral

A

Lung cancer

(a) “Sentral” for squamous cell and small cell
(b) Peripheral- adenocarcinoma

66
Q

Two type of lung cancers that stain chromogranin positive

A

Both small cell carcinoma (poorly differentiated from neuroendocrine cells) and carcinoid tumor (well differentiate neuroendocrine cells in nests) stain chromogranin positive

67
Q

Clinical presentation of SVC syndrome

A

SVC obstruction (ex: from lung cancer) causes distended head and neck veins w/ edema, blue discoloration of arms and face (can’t drain venous blood out)

68
Q

Unique place that lung cancer likes to met to

A

Adrenal glands

69
Q

Clinical presentation of mesothelioma

A

Recurrent pleural effusions (b/c mesothelial cells normally secrete fluid to keep the pleural space lubricated), dyspnea, chest pain

70
Q

MC lung cancer in

(a) Nonsmokers
(b) Male smokers
(c) Female smokers

A

MC lung cancer in

(a) Nonsmokers = adenocarcinoma
(b) Male smokers = squamous cell carcinoma
(c) Female smokers = adenocarcinoma

71
Q

Histologic finding of large cell carcinoma of the lungs

A

Poorly differentiated large cells

  • no keratin pearls or intracellular bridges (seen in squamous cell carcinoma)
  • no glands or mucin (as seen in adenocarcinoma)
72
Q

MC congenital renal anomaly

A

MC congenital renal anomaly = horseshoe kidney

-fused at lower poles

73
Q

Clinical presentation of unilateral renal agenesis

A

Unilateral renal agenesis asymptomatic at birth- causes hypertrophy of the other kidney, then over time hyperfiltration of the single kidney increases risk of renal failure later in life

74
Q

Clinical presentation of b/l renal agenesis

A

B/l renal agenesis = no urine = oligohydramnios => Potter sequence

  • pulmonary hypoplasia (b/c lungs need fluid to stretch them for proper development)
  • flat facies w/ low set ears and limb/extremity defects (b/c w/o fluid to float in these things get smushed against maternal structures)
75
Q

Potter sequence

A

B/l renal agenesis or b/l renal defect = no urine = oligohydramnios => Potter sequence

  • pulmonary hypoplasia (b/c lungs need fluid to stretch them for proper development)
  • flat facies w/ low set ears and limb/extremity defects (b/c w/o fluid to float in these things get smushed against maternal structures)
76
Q

Name a noninherited caused of cystic kidney disease

(a) How to differentiate from PKD

A

Noninherited cystic kidney disease = Multicystic Dysplastic kidney, noninherited but congenital malformation of the renal parenchyma
-cysts and abnormal tissue (often cartilage)

(a) PKD is more commonly b/l (but dysplastic kidney can be b/l MC unilateral). presence of abnormal tissue in dysplastic kidney

77
Q

Differentiate the mode of inheritance of the two forms of polycystic kidney disease

(a) Presents in infants
(b) Presents in young adults

A

PKD

(a) Aut recessive form presents in infants w/ worsening renal failure and HTN
(b) Aut dom form (APKD1 or APKD2 mutation) presents in young adults w/ HTN, hematuria, and worsening renal failure
- b/c cysts develop over time (not present at birth)

78
Q

Autosomal recessive polycystic kidney disease

(a) Age of presentation
(b) 2 associated conditions

A

Aut recessive PKD

(a) Presents in infants w/ worsening renal failure and HTN b/c the cysts are present at birth
(b) ‘Cysts in kidney and liver’- associated hepatic cysts and congenital hepatic fibrosis that leads to portal HTN

79
Q

Autosomal dominant polycystic kidney disease

(a) Age of presentation
(b) Associated conditions

A

Aut dom PKD 2/2 mutation in APKD1 or APKD2

(a) Presents in young adults b/c cysts aren’t present at birth, develop over time, then present w/ HTN, hematuria, and worsening renal failure

(b) ‘Cysts in kidney, liver, and brain’- associated hepatic cysts and berry aneurysm (cystic dilation of intracranial arteries)
- also associated mitral valve prolapse

80
Q

How to differentiate polycystic kidney disease from medullary cystic kidney disease

A

Both are inherited cystic kidney diseases

Medullary kidney disease- cysts only develop in the medullary collecting ducts, vs. in both medulla and cortex of PKD

Medullary cystic disease- parenchymal fibrosis leads to shrunken kidneys, vs. enlarged b/l kidneys in PKD

81
Q

Explain the BUN:Cr ratio seen in prerenal azotemia

A

Both BUN and Cr are normally filtered, but Cr doesn’t really get reabsorbed (most excreted in urine) while BUN gets actively resorbed

So when tubules are functioning properly, BUN:Cr ratio is about 15:1

Then in prerenal azotemia (low flow), renin released –> high aldo so reabsorb more water and BUN follows so BUN:Cr > 15, indicating tubules are functioning properly

82
Q

FENa seen in

(a) Prerenal azotemia
(b) Early postrenal azotemia
(c) ATN

A

FENa (fractional excretion of Na)

(a,b) Tubules are functioning properly so FENa is under 1%
(c) Tubules are damaged => can’t properly reabsorb Na => FENa over 2%

83
Q

Give an etiology of

(a) Prerenal azotemia
(b) Postrenal azotemia

A

Etiology

(a) Prerenal azotema- low flow state (hypovolemia), dehydration, low cardiac output (heart failure)
(b) Postrenal azotemia- ureteral obstruction, bladder outlet obstruction

84
Q

Urine osmolality in

(a) Prerenal azotemia
(b) Early postrenal azotemia
(c) ATN

A

Urine osmolality

(a,b) Tubules working properly to concentrate urine so Uosms over 500

(c) ATN tubules are damaged and can’t properly concentrate urine, Uosm under 500

85
Q

Differentiate the findings in early vs. long-standing postrenal azotemia

A

Postrenal azotemia- in the beginning tubules are functioning properly so FENa under 1% and Uosm over 500, then over time from obstruction pressure the tubules get damaged => see FENa rise and Uosm decrease (b/c tubules can no longer function to concentrate urine)

86
Q

MC cause of acute intrarenal azotemia

A

MC cause of intrarenal azotemia = acute tubular necrosis (more common than acute interstitial nephritis)

87
Q

Explain the physiology of ATN

(a) BUN:Cr ratio
(b) FENa

A

ATN: injury and necrosis of the tubular epithelial cells causes necrotic cells to plug the tubules, this obstruction decreases GFR

(a) BUN:Cr ratio under 15 b/c tubules not functioning so can’t resorb BUN
(c) FENa over 2% b/c decreased Na reabsorption

88
Q

Which part of the nephron is most susceptible to ischemic vs. nephrotoxic causes of ATN

A

Proximal tubule and medullary segment of thick ascending limb are most susceptible to toxic damage b/c highest O2 (ATP) requirement

Proximal tubule gets hit first by the toxin => most susceptible to nephrotoxic agents

89
Q

MC toxic agent responsible for ATN

A

MC toxic agent = aminoglycosides (Streptomycin, Gentamycin, Tobramycin, Amikacin)

90
Q

Type of AKI caused by radiocontrast dye

A

Radioconstrast dye is a toxin that causes necrosis of the tubules => nephrotoxic ATN

91
Q

How to reduce the risk of urinate induced ATN 2/2 chemotherapy administration

A

Tumor lysis syndrome can release tons of urate that is toxic to the nephron => administer chemo with tons of fluid and allopurinol (inhibit urate production) to reduce risk of ATN w/ chemo

92
Q

Ethylene glycol (antifreeze) causes what kind of AKI?

(a) What kind of urine crystals?

A

Ethylene glycol => nephrotoxic ATN

(a) Oxalate crystlas

93
Q

Metabolic abnormalities caused by ATN

A

ATN => hyperkalemia and anion-gap metabolic acidosis 2/2 reduced excretion of K+ and H+

94
Q

How long does ATN vs. AIN last?

A

Oliguria in ATN can last 2-3 weeks b/c tubular cells are stable cells- means they can re-enter the cell cycle but they’re not actively dividing, so takes a bit of time for tubular cells to reenter the cell cycle and regenerate

AIN is a hypersensitivity rxn => resolves immediately w/ cessation of the drug

95
Q

What type of reaction is AIN?

(a) 3 main causes

A

AIN = drug-induced hypersensitivity rxn involving interstitium and tubules

(a) NSAIDs, penicillins, diuretics

96
Q

Clinical presentation of AIN

(a) Main lab finding
(b) Most feared complication

A

AIN presents as oliguria, fever, and rash days to weeks after starting a drug

(a) Eosinophils may be seen in urine
(b) Renal papillary necrosis = necrosis of renal papillae

97
Q

Name some causes of papillary necrosis

A

Necrosis of the renal papillae presents w/ gross hematuria and flank pain, can be from recurrent AIN drug-induced hypersensitivity rxns

Causes:
-chronic analgesic (ex: ASA) use

98
Q

Young adult p/w hematuria
-father w/ died of intracranial hemorrhage

Dx?

A

Autosomal condition w/ renal cysts and berry aneurysms = aut dom polycystic kidney disease

Presents in young adults w/ worsening renal failure, HTN, hematuria b/c cysts need time to develop (not present at birth like in aut recessive PKD), associated hepatic cysts, berry aneurysms, and mitral valve prolapse

99
Q

Brown muddy casts

A

UA finding of acute tubular necrosis

100
Q

Brown muddy casts

A

UA finding of acute tubular necrosis

101
Q

MC cause of

(a) Nephritic
(b) Nephrotic

syndrome in lupus pts

A

SLE pts

(a) Nephritic syndrome = diffuse proliferative glomerulonephritis- granular (immune complex) IF = IC are subendothelial
(b) Nephrotic syndrome = membranous nephropathy = IC are subepithelial

102
Q

Clinical manifestations of nephrotic syndrome

A

Nephrotic syndrome: proteinuria of over 3.5 g/day

  • hypoalbuminemia => pitting edema (2/2 loss of interstitial oncotic pressure)
  • hypogammaglobulinemia => increased risk of infection
  • pee out tons of ATIII => hypercoagulable state
  • hyperlipidema and hypercholesterol b/c liver realized blood is ‘thin’ (low proteins) so pumps out thickeners
103
Q

Nephrotic vs. nephritic syndrome

(a) Amount of protein in urine
(b) Casts found in urine

A

Nephrotic

(a) over 3.5 g/day of proteinuria
(b) Not usually, but can see fatty casts in urine 2/2 dyslipidemia b/c liver pumps out lipids 2/2 thin blood (low protein)

Nephritic

(a) Under 3.5 g/day
(b) See RBC casts (sign of glomerular bleeding) and dysmorphic RBCs in the urine b/c characterized by glomerular inflammation and bleeding

104
Q

Minimal change disease is associated w/ what malignancy?

A

MCD is associated w/ Hodgkin lymphoma

Podocyte damage in MCD is 2/2 cytokine release, and Reed-Sternberg cells in HL release TONS of cytokines

105
Q

MC cause of nephrotic syndrome in

(a) Hispanics and African Americans
(b) Caucasians

(c) MC nephropathy worldwide

A

Nephrotic syndrome in

(a) Hispanics and African Americans = Focal segmental glomerulosclerosis- no immune complexes, get focal and segmental sclerosis of glomerulus
(b) Caucasians = Membranous Nephropathy where immune complexes deposit subepithelialy
(c) MC nephropathy worldwide = IgA nephropathy (nephritic)

106
Q

Nephrotic syndrome associated w/

(a) HBV and HCV
(b) SLE
(c) HIV, heroin use
(d) SCD

A

Nephrotic syndrome associated w/

(a) Hep B and C = type I membranoproliferative glomerulonephritis (MPGN)
-type I has subendothelial deposits
(b) SLE more commonly nephritic syndrome, but if nephrotic = membranous nephropathy
(c,d) HIV, heroin use, and SCD associated w/ FSGS (focal segmental glomeruloscerlsosi

107
Q

Tx of nephrotic syndrome as a whole

A

All except MCD are minimally responsive to steroids

  • So FSGS, membraneous nephropathy, MPGN have poor response to steroids
  • for diabetes give ACEi to slow down hyperfiltration damage
108
Q

Dx to suspect when young adult w/ podocyte effacement on EM does not respond to steroid tx

A

Podocyte effacement Ddx = MCD and FSGS

but MCD mroe common in children and has excellent response to steroids, so if non-responsive to steroids think more FSGS

109
Q

Nephrotic syndrome w/

(a) Spike and dome appearance on EM
(b) Tram track appearance

A

Nephritic syndrome w/

(a) Spike and dome appearance = membranous nephropathy
- due to immune complex deposition subepithelially, podocytes lay more basement membrane which domes over the immune complex

(b) Tram track appearance of MPGN b/c proliferation of mesangial cell cuts the immune complex in half like a tram track

110
Q

Which nephrotic syndrome is associated w/ C3 nephritic factor?

A

C3 nephritic factor = autoantibody that stabilizes C3 convertase => overactivation of complement b/c usually C3 convertase makes C3a and C3b rather quickly so that C3 doesn’t remain active

Overactivation of complement => inflammation and low circulating C3 seen in type II membranoproliferative glomerulonephritis

111
Q

First pathological step in diabetic nephropathy

A

Nonenzymatic glycosylation of the vascular basement membrane

112
Q

Describe the mechanism of diabetic nephropathy

(a) What causes microalbuminemia?

A

Nonenzymatic glycosylation of the basement membrane causing hyaline arteriolosclerosis

(a) Preferential hyaline arteriolosclerosis (thickening) of efferent arteriole increases the glomerular filtration pressure which causes hyperfiltration
Hyperfiltration injury => microalbuminuria that eventually progresses to nephrotic syndrome

113
Q

Mechanism by which ACEi decreases risk of diabetic nephropathy

A

In diabetic nephropathy there is preferential hyaline arteriolosclerosis of the efferent arteriole which increases filtration pressure, eventually damaging glomerulus => nephrotic syndrome

ATII preferentially vasoconstricts efferent arteriole- so worsens this filtration pressure => ACEi slows progression of hyperfiltration-induced glomerular damage

114
Q

Explain the mechanism by immune complex damage causes inflammation seen in nephrotic syndrome

A

Immune complexes deposit which activates complement, then C5a goes on to activate neutrophils which mediate inflammatory damage

115
Q

Which strains of streptococcus can cause nephritic syndrome

A

Group A strep strains that are nephritogenic are the ones that carry M-protein virulence factor

W/o M-protein the strain can’t cause PSGN
-usually strains that cause impetigo and strep pharyngitis have M-protein

116
Q

Poor prognostic factor for post-strep GN

A

Older age! Only 1% of children progress to renal failure, while almost 25% of adults develop rapid progressive glomerulonephritis

117
Q

What is rapid progressive glomerulonephritis?

(a) Timeline to renal failure
(b) Nephrotic or nephritic?
(c) Typical H&E finding
(d) How to determine etiology

A

RPGN

(a) Rapid as in weeks to months until progresses to renal failure
(b) Nephritic syndrome- inflammation and bleeding of the glomerulus
(c) Crescentic formation in glomerulus
(d) Determine etiology by immunofluorescence (see if and where immune complexes are)

118
Q

MC type of renal disease in SLE

A

MC renal disease in SLE = diffuse proliferative glomerulonephritis which is a subtype of rapidly progressive glomerulonephritis (nephritic syndrome)

119
Q

Name the dx when IF of rapidly progressive glomerulonephritis shows

(a) No ICs
(b) Linear pattern
(c) Granular pattern

A

Immunofloresence

(a) No immune complexes = pauci-immune = vasculitis etiology: Wegener granulomatosis, microscopic polyangiitis, Churg-Strauss syndrome
(b) Linear pattern = anti-basement Ab seen in Goodpasture syndrome
(c) Granular pattern = IC deposition seen in post-strep Gn and diffuse proliferative glomerulonephritis

120
Q

Differentiate the 3 pauci-immune etiologies of rapidly progressive glomerulonephritis

A

Rapidly progressive glomerulonephritis (nephritic syndrome w/ crescentic pattern that progresses to renal failure w/in weeks to months) that doesn’t have immune complex deposition on immunofluorescence = pauci-immune

c-ANCA = Wegeners granulomatsosi

p-ANCA = Microscopic polyangiitis and Churg-Strauss

121
Q

Clinical presentation of IgA Nephropathy

A

IgA nephropathy presents w/ episodic microscopic hematuria (RBC casts) following mucosal infection

Mucosal infection increases IgA production => more IgA immune complexes deposit in mesangium of glomerulus => RBC casts in urine

122
Q

Inheritable cause of nephritic syndrome

A

Alport syndrome = X-linked defect in collagen IV causing nephritic syndrome w/ hearing and visual difficulties

123
Q

Mechanism of poststreptococcal glomerulonephritis

A

Immune complex deposition subepithelially secondary to M-protein virulence factor of Group A strep

124
Q

How to differentiate p-ANCA pauci-immune rapidly progressive glomerulonephritis

A

Two p-ANCA positive causes of RPGN = Microscopic polyangiitis and Churg-Strauss

Churg-Strauss will have granulomatous inflammation, eosinophilia, and asthma (differentiating factors)

125
Q

Clinical features of cystitis vs. pyelonephritis

A

Cystitis- urinary frequency and dysuria (pain w/ urination) but w/o the systemic features (fever) seen w/ pyelo

126
Q

Cystitis

(a) UA finding
(b) Dipstick
(c) Cx gold standard

A

Cystitis

(a) UA finding: over 10 WBC per high power field
(b) Dipstick positive for nitrates (made by bacteria) and leukocyte esterase
(c) Cx w/ over 100k colonies = gold standard

127
Q

Name 4 organisms responsible for cystitis in addition to E. Coli

A

Cystitis

80% E. Coli 
Staph saprophyticus
Klebsiella
Proteus mirabilis 
Enterococcus faecalis
128
Q

Which organism causes cystitis w/ alkaline urine and ammonia scent

A

Proteus mirabilis => alkaine urine w/ ammonia scent

129
Q

What lab findings suggest urethritis over cystitis?

(a) Organisms responsible

A

Sterile pyruria = over 10 WBC/hpf and positive leuk esterase but w/ negative urine culture

(a) Urethritis think neisseria gonorrhea and chlamydia trachomatis

130
Q

3 MC causes of Pyelonephritis

A

Pyelo
90% E. coli
Enterococcus faecalis
Klebsiella

131
Q

2 causes of chronic pyelonephritis

(a) What type of casts seen in urine

A

Chronic pyelo 2/2 VUR or obstruction (BPH, cervical carcinoma)

(a) Waxy casts on UA indicative of chronic pyelo

132
Q

What causes ‘thyroidization’ of the kidney

A

Chronic pyelonephritis- atrophic tubules contain eosinophilic proteinaceous material that resembles colloid seen in thyroid follicles

133
Q

Tx of the MC type of nephrolithilasis

A

MC kidney stone = calcium oxalate and/or calcium phosphate

Tx by decreasing calcium in urine w/ HCTZ = Ca2+ sparing diuretic

134
Q

2nd MC type of kidney stone

(a) Cause
(b) Why does tx involve surgery

A

2nd MC kidney stone = ammonium magnesium phosphate stone

(a) MC caused by urease-positive organism infection (proteus vulgaris or Klebsiella) b/c the alkaline urine leads to formation of stone
(b) B/c classically causes a staghorn calculi in the renal calyce which acts as a nidus for UTI => need to remove the huge stone then also tx w/ abx

135
Q

Which types of kidney stones are visible on imaging?

A

2 MC types (calcium oxalate/phosphate and ammonium magnesium phosphate) stones are radiopaque = visible on Xray

While uric acid stones (about 5% of kidney stones) are radiolucent = won’t show up on Xray

136
Q

RF for uric acid kidney stones

A

Hot arid climates, low urine volume (b/c low volume means high concentration of solute), acidic pH, hyperuricemia (leukemia, myeloproliferative d/o, gout)

137
Q

Tx for uric acid kidney stones

A

Hydration and alkalinization of urine (w/ potassium bicarbonate)
-b/c acidic pH increases uric acid precipitation

Allopurinol if pt has gout

138
Q

Type of kidney stone more commonly seen in children than adults

A

Cystine kidney stone MC in children than adults b/c of cystinuria = genetic defect in tubules from decreased ability to reabsorb of cysteine

139
Q

Explain these clinical features of chronic renal failure

(a) HTN
(b) pH abnormality
(c) Hypercoagulability

A

Chronic renal failure

(a) HTN b/c of salt and water retention
(b) Hyperkalmeia w/ metabolic acidosis (not excreting H+ out collecting duct)
(c) Hypercoagulability b/c uremia causes plt dysfunction

140
Q

Explain these clinical features of chronic renal failure

(a) Anemia
(b) Hypocalcemia
(c) Osteitis fibrosa

A

Chronic renal failure

(a) Anemia 2/2 lack of EPO production by renal peritubular interstitial cells

141
Q

What cancer does dialysis increase risk for?

A

Renal cell carcinoma

142
Q

Renal neoplasm associated w/ tuberous sclerosis

A

Angiomyolipoma = hamartoma of BV (angio), smooth muscle (myo), and fat (lipo)

143
Q

Renal cell carcinoma

(a) Cell of origin
(b) MC clinical symptom
(c) Right or left vericocele

A

RCC

(a) Malignant epithelial tumor of tubular cells
(b) Hematura = MC symptom, classic triad hematuria palpable mass and flank pain only present all 3 10% of the time
(c) Left vericocele b/c RCC likes to spread to the renal vein, L renal vein involvement blocks drainage of left renal vein

144
Q

Name the paraneoplastic syndromes that can be seen 2/2 RCC

A

Renal cell carcinoma can produce EPO, renin, PTHrP, or ACTH

-so polycythemia, HTN, hypercalcemia, Cushings

145
Q

Gene mutation seen in RCC

A

Pathogenesis of RCC = loss of VHL tumor suppressor gene => increased IGF-1 that promotes growth

146
Q

Major RF for sporadic renal cell carcinoma

(a) Location of sporadic form

A

Smoking = major RF

(a) Sporadic form typically in males over 60, arises as single tumor in upper pole

147
Q

Differentiate sporadic from hereditary renal cell carcinoma

A

Hereditary tumors arise in younger adults, not associated w/ smoking, and are often bilateral

ex: VHL disease = aut dom inactivation of VHL gene

148
Q

Unique feature of T-staging for renal cell carcinoma

A

Size of tumor but also includes involvement of the renal vein (very common)

149
Q

Composition of Wilms tumor

(a) Average age

A

Wilms tumor = malignant tumor comprised of blastema = immature kidney mesenchyme that forms primitive glomeruli, tubules,and stromal cells

(a) 3 yoa

150
Q

Renal cell carcinoma MC subtype

(a) Gross pathologic feature
(b) Histologic appearance

A

RCC MC subtype = clear cell

(a) Grossly yellow mass
(b) MC subtype shows clear cytoplasm

151
Q

Clinical presentation of Wilms tumor

A

Wilms tumor = malignant kidney tumor of blastema presents as large unilateral flank mass (lateral, not central) p/w hematuria and hypertension (HTN 2/2 renin secretion)

152
Q

Long term cyclophosphamide increases risk of what cancer?

A

Long term cyclophosphamide increases risk of urothelial (transitional) cell cancer- MC of the bladder

153
Q

Urothelial carcinoma

(a) MC location
(b) Why often multifocal

A

Urothelial carcinoma = transitional cell carcinoma of the lower urinary tract

(a) MC bladder
(b) Field defect b/c the carcinogen hits the entire urothelium => tumors often multifocal and recur

154
Q

What is a necessary precursor lesion to squamous cell carcinoma of the bladder?

A

Bladder is transitional epithelium, therefore squamous metaplasaia must occur before SCC can arise

Squamous cell metaplasia from chronic irritation of the urothelium
ex: from chronic cystitis, Schistosoma haematobium infection (Egyptian, middle eastern male), long-standing nephrolithiasis

155
Q

Embryological defect that increases risk of bladder adenocarcinoma

A

Urachal remnant (urachus drains waste from fetal bladder into yolk sac) can form adnocarcinoma of the bladder- tumor develops at the dome of the bladder

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