Pathology Flashcards

1
Q

Most common site of nasal polyp

A

middle meatus

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

Most common nose bleed

A

anteroinferior nasal septum

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

Life threatening hemorrhage in nose

Artery involved?

A

posterior segment

sphenopalatine artery a branch of maxillary artery

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

Kiesselbach plexus formed by

A

LEGS: superior Labial artery, anterior and posterior Ethmoidal arteries, Greater palatine artery, Sphenopalatine artery.

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

Rapidly declining effect of topical nasal decongestant is due to

A

Tachyphylaxis

↓production of endogenous norepinephrine

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

lab test used clinically to rule out DVT:

Imaging test of choice is :

A

►D-dimer

►compression ultrasound with Doppler.

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

Most pulmonary emboli arise from

A

proximal deep veins of lower extremity.

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

______ is imaging test of choice for PE

A

CT pulmonary angiography

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

______ is imaging test of choice for PE in CKD

A

ventilation/perfusion scan

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

Changes in flow-volume curve in PE

A

normal, as there is no effect on ventilation. only effect on perfusion

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

_____ doesnot remain constant after 30 years even in non-smokers

A

FEV1

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

Hypercoagulable state: Pregnancy changes

A

Compression of IVC and iliac vein
↑ production of coagulation factors
↓ Protein S
Protein C resistance

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

Ruptured alveoli allow tracking of air into the mediastinum via

A

peribronchial and perivascular sheaths

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

Pneumomediastinum Clinical features:

A

Clinical features: chest pain, dyspnea, voice change, subcutaneous emphysema, ⊕ Hamman sign (crepitus on cardiac auscultation).

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

Chronic mediastinitis—also known as ____

Common cause

A

fibrosing mediastinitis; due to proliferation of connective tissue in mediastinum.

Histoplasma capsulatum is common cause

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

Posterior mediastinal masses—

A

►neurogenic tumor (eg, neurofibroma),

►multiple myeloma.

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

______ increase respiratory rate in response to pathologic alveolar process (eg. pulmonary edema, pneumonia)

A

Alveolar juxtacapillary receptors

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

_______ is the major cause of dyspnea and exercise limitation in COPD

A

Dynamic hyperinflation

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

Dynamic hyperinflation

A

Hyperinflation in COPD during exercise. patient requires extra time for exhalation → increasing trapped air during rapid breathing → ↓tidal volume

20
Q

Depth and rate of respiration are controlled by _____ based on _______

A

medullary respiratory center

based on inputs from central and peripheral chemoreceptors

21
Q

Damage in late phase of asthma is due to

A

Major basic protein released by eosinophils

22
Q

Damage in early phase of asthma due to

A

PREFORMED Histamine

GENERATION of LT C4,D4,E4

23
Q

Most common cause of COPD exacerbation is

A
  1. Viral (rhino, influenza, parainfluenza)

2. Bacterial

24
Q

Current Jelly & Rusty coloured sputum is due to

A

Extravasation of RBCs and Hb in sputum

25
Q

ABPA microscopy

A

Fungi donot invade mucosa and non-caseating granulomas would not be seen

26
Q

Air enters pleural space but cannot exit.

A

tension pneumothorax

27
Q

tension pneumothorax complication

A

May lead to increased intrathoracic pressure →mediastinal displacement →kinking of IVC →↓venous return →→cardiac output.

28
Q

Obstructive hyperinflation occurs in

A

partial airway obstruction (dilated during inspiration but closed during expiration)

29
Q

Atelectasis X-ray finding

A

Opacification

30
Q

Partial obstruction of large airway physical finding

A

A focal, monophasic wheeze

31
Q

Diffuse alveolar hemorrhage: Restrictive or Obstructive pattern?

A

dilutes surfactant → alveolar atelectasis → Restrictive flow-volume pattern

32
Q

Atelectasis: Restrictive or Obstructive pattern?

A

Restrictive flow-volume pattern

33
Q

Atelectasis etiologies:

A

Obstructive
Compressive
Contraction
Adhesive: due to lack of surfactant

34
Q

Hepatic hydrothorax

A

ascites forced into right sided pleural cavity through fenestrations in diaphragm (transudative)

35
Q

Mesothelioma Histology

A

Psammoma bodies seen on histology.
Calretinin and cytokeratin 5/6 ⊕, pancytokeratin
cuboidal/spindle shaped cells

36
Q

BOOP 4 features

A

Foamy macrophages
Masson bodies
Interstitial collagen deposition
Uniform fibroblastic proliferation

37
Q

PE physical exam

A

Diffuse crackles, ronchi, scattered wheeze

38
Q

Progressive hypoxemia refractory to oxygen therapy

A

ARDS

39
Q

ARDS symptoms

A

►Abnormal chest X-ray (bilateral lung opacities)
►Respiratory failure within 1 week of alveolar insult
►Decreased Pao2/Fio2 (ratio < 300, hypoxemia due to intrapulmonary shunting and diffusion abnormalities)
►Symptoms of respiratory failure are not due to HF/fluid overload

40
Q

Non cardiogenic pulmonary edema seen in

A

ARDS

High altitude

41
Q

OSA is primarily a problem of _____ not _____

A

pharynx, not larynx

42
Q

Most common indicator of obesity hypoventilation syndrome is

A

↓ Expiratory reserve volume
↓ Functional residual capacity
Normal RV

43
Q

Obesity hypoventilation syndrome is also known as
During waking hours
During sleep

A

►Also known as Pickwickian syndrome.

► ↑Paco2 during waking hours (retention); ↓Pao2 and ↑Paco2 during sleep.

44
Q

Pulmonary hypertension: death from

A

decompensated cor pulmonale.

45
Q

Pulmonary arterial hypertension: Heritable PAH can be due to

A

an inactivating mutation in BMPR2 gene (normally inhibits vascular smooth muscle proliferation)

46
Q

Portal HTN causes pulmonary HTN, how?

A

Portopulmonary HTN
►Portal HTN → portosystemic shunt → unmetabolized substances into pulmonary circulation (serotonin) → smooth muscle hyperplasia of pulmonary capillaries → pulmonary HTN
► ↑hydrostatic pressure on portal vein releases endothelin →portosytemic shunt → pulmonary HTN

47
Q

Silicosis histology:

A

Nodules composed of whorled collagen fibers and dust laden macrophages