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deck_15291969 Flashcards

1
Q

pathogenesis of atherosclerosis

A
  • endothelial injury → increased permeability → leukocyte adhesion & macrophage activation
  • lipid deposition in damaged intima
  • macrophages engulf lipids → lipid accumulation → fatty streaks (EARLY)
  • macrophages secrete cytokines and growth factor → ECM synthesis esp collagen
  • collagen synthesis forms dense fibrous cap over plaque → white & hard (ESTABLISHED)
  • collagenisation affect tunica media → disrupt elastic intima
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2
Q

MI – how MI leads to pulmonary & ankle oedema

A

death of heart muscles → LV pump failure
backward failure → LA dilation → pulmonary hypertension → pulmonary congestion → pulmonary oedema
left side fail → RV failure → systemic & portal congestion → ankle oedema

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3
Q

complications of MI

A

Myocardial rupture
Congestive heart failure
Fibrosis
Aneurysm
Thrombus
Pericarditis
Ruptured papillary muscle
Arrhythmia
Contractile dysfunciton

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4
Q

modifiable risk factors of MI

A

smoking
hyperlipidemia
hypertension
diabetes

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5
Q

non-modifiable risk factors of MI

A

age
gender
family history
genetics

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6
Q

infective endocarditis (what? cause? symptoms?)

A

infection of valves
- acute: S aureus
- subacute: Viridans strep

form vegetation → destroy tissues

symptoms: fever, chills, heart murmur

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7
Q

rheumatic heart disease

A

abnormal immune response (to group A Strep Pharyngitis)
- inflammation & damage to heart valves → stenosis and regurgitation

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8
Q

causes of hyperthyroidism

A

primary: Graves, toxic multi nodular goitre, toxic neoplasm
secondary: pituitary hyperfunction

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9
Q

causes of hypothyroidism

A

primary: hashimoto (most common), iatrogenic
secondary: pituitary failure

cretinism (congenital in children) – dietary iodine deficiency

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10
Q

symptoms + biochemical signs of hyperthyroidism

A

weight loss
hot - heat intolerance
oligomenorrhoea (infrequent period)
diarrhoea
irritable mental state
increased appetites

high T3, T4
low TSH

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11
Q

symptoms + biochemical signs of hypothyroidism

A

weight gain
cold intolerance
menorrhagia (heavy period)
constipation
mental slowness
decreased appetite

low T3, T4
high TSH (primary), low TSH (secondary)

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12
Q

pathogenesis of graves

A
  • autoantibodies bind & activate TSH receptor
  • release of T3, T4
  • increase cellularity & hyperplasia of gland
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13
Q

gross features of graves

A
  • diffuse enlargement
  • red meaty cut surface
  • smooth & soft gland, intact capsule

histology:
- follicular cells tall, columnar, crowded – pseudopapillae
- inflammatory cells

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14
Q

gross features of hashimoto

A
  • pale
  • enlarged

histology:
- lymphoid follicles
- hurthle cell changes

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15
Q

which thyroid carcinoma metastasise via bloodstream

A

follicular carcinoma

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16
Q

which thyroid carcinoma metastasise via lymphatics (LN)

A

papillary carcinoma

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17
Q

medullary carcinoma associated with??

A

MEN (multiple endocrine neoplasia)
- younger patient

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18
Q

diagnosis for single thyroid nodule

A

follicular adenoma
follicular carcinoma
papillary carcinoma
anaplastic carcinoma
medullary carcinoma

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19
Q

features of papillary carcinoma

A
  • nuclear features: finely dispersed chromatin, nuclear grooves, pseudo inclusions
  • papillae with fibrovascular cores
  • psammoma bodies
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20
Q

MEN 1 associated with which gene mutation

A

MENIN gene mutation

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21
Q

MEN 2 associated with which gene mutation

A

RET gene mutation

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22
Q

MEN 1 clinical feature

A

PHAIG
prolactinoma - excessive breast milk production
hyperparathyroidism - hypercalcemia
adrenal adenoma – cushing syndrome
insulinoma
gastrinoma - gastric ulceration

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23
Q

MEN 2B clinical feature

A
  • mucosal neuroma syndrome (growth around nerves of mucous membranes)
  • marfanoid syndrome (long limbs, loose joints, curved spine)
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24
Q

role of PTH

A

increase Ca levels by
- ↑ bone resorption by osteoblasts
- ↑ renal tubular absorption
- ↑ intestinal absorption (mediated by Vit D, PTH ↑ its synthesis)

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25
Q

causes of hyperparathyroidism

A

primary
- parathyroid adenoma (MOST COMMON) / carcinoma – 1 gland enlarged
- parathyroid hyperplasia – >1 glands enlarged

secondary
- renal failure (kidney too much phosphate reabsorption => form insoluble calcium phosphate => ↓ serum Ca2+ => ↑ PTH)

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26
Q

effects/consequences of parathyroidism

A
  • renal & urinary calculi
  • osteitis fibrous cystica
  • hypertension
  • pancreatitis
  • peptic ulcer
  • metastatic calcification
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27
Q

causes of hypoparathyroidism

A

iatrogenic (surgery)
autoimmune

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28
Q

causes of adrenal hyperfunction

A

primary
- adrenal adenoma/carcinoma
- adrenal hyperplasia

secondary
- pituitary adenoma

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29
Q

Cushing syndrome clinical features

A

cushing is due to increase in cortisol

  1. adrenal tumour/hyperplasia
  2. moon face, buffalo hump, obesity
  3. hyperglycaemia
  4. hypertension
  5. osteoporosis
  6. thin wrinkled skin, abdominal striae
  7. muscle weakness
  8. emotional disturbance
  9. skin ulcers (poor wound healing)
  10. amenorrhea
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30
Q

causes of adrenal hypofunction

A

primary
- iatrogenic (surgery)
- autoimmune
- haemorrhage (blood vessels in adrenal gland rupture)
- infections: TB, histoplasmosis
- metastatic tumours

secondary
- pituitary disease

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31
Q

effects of adrenal hypofunction

A
  • weight loss
  • muscle weakness
  • low BP
  • poor immune response
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32
Q

polycythaemia

A

too much RBCs
- associated with hypoxia – living at high altitudes

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33
Q

causes of anaemia

A

too few RBC
- decrease production: iron/B12/folate deficiencies
- bleeding
- increased destruction: Hb defects (sickle cell / thalassaemia), enzyme defects (G6PD)

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34
Q

symptoms of anaemia

A

pallor
weakness
dizziness/syncope
palpitation, chest pain, shortness of breath

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35
Q

leukocytosis – following associated with what
- neutrophilia
- eosinophilia
- monocytosis
- lymphocytosis

A
  • neutrophilia: infection, tissue necrosis
  • eosinophilia: allergies, parasitic infection
  • monocytosis: chronic infections (eg. TB), autoimmune disease
  • lymphocytosis: viral infections, TB
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36
Q

thrombocytosis – what? and causes

A

too many platelets

primary: neoplastic
secondary:
- hemorrhage
- splenectomy
- infections
- inflammatory conditions (autoimmune disease)

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37
Q

effects of thrombocytosis

A

thrombosis
bruising
bleeding

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38
Q

thrombocytopenia

A

too few platelets
caused by
- bone marrow damage (Chemo/radiotherapy),
- autoimmune disease
- hypersplenism (splenomegaly)
- increased consumption (shock, burns, sepsis)

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39
Q

effects of thrombocytopenia

A
  • petechiae
  • bruising
  • bleeding (nose bleed; internal bleeds)
  • prolonged bleeding
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40
Q

causes haemophilia (inherited/acquired)

A

inherited coagulation factor deficiency
- haemophilia A: factor 8
- haemophilia B: factor 9
- Von Willebrand’s disease: VW factor

acquired disorders:
- liver disease – ↓ clotting factor
- Vit K deficiency

41
Q

leukemia types

A

ALL - acute lymphoblastic leukaemia: C1
CLL - chronic lymphoid leukaemia: A1
AML - acute myeloblastic leukaemia: C2, A1
CML - chronic myeloid leukaemia

42
Q

clinical signs for benign vs malignant LN

A

BENIGN vs MALIGNANT
tender | non-tender
discrete | discrete/matted
small | large
mobile/bilateral | fixed to underlying structures

43
Q

causes of benign lymphoma

A
  • bacterial
  • viral (EBV)
  • granulomatous (TB, bartonella hanselae → cat-scratch disease)
  • autoimmune disease (SLE)
  • sarcoidosis
44
Q

causes of malignant lymphoma

A

Primary: non-hodgkin lymphoma & Hodgkin lymphoma

secondary: metastasise from NPC, SCC, breast carcinoma

45
Q

Identifying Source of Tumour for Tx

A

Type:
- Carcinomas tend to spread via lymphatics => LN metastasis more likely
- Sarcomas tend to spread via blood => LN metastasis less likely

Location of LN:
- Upper cervical: upper GIT, nasopharynx
- Supraclavicular: lung, breast
- Inguinal: external genital organs, lower limbs

Immunohistochemistry:
- Detect small deposits of tumour
- Distinguish btw primary & secondary tumours
- Specific markers (antibodies) to identify primary site of metastases

46
Q

which lymphoma associated with EBV

A

hodgkin lymphoma

47
Q

non-hodgkin lymphoma
- associated with which age group
- histo

A
  • 2 peaks: young adults & elderly
  • Reed Sternberg cell (OWL EYES)
48
Q

gross features of SCC

A

masses of necrosis
ulcers with rolled margins

histo: keratinised growing pattern, atypia at base, irregular stromal invasion

49
Q

risk factors of SCC

A

smoking, alcohol
tobacco chewing, betel nut chewing
HPV esp type 16

50
Q

causes of chronic gastritis

A
  • H. pylori
  • autoimmune: pernicious anemia
  • toxic: smoking/alcohol
  • post surgical: bile reflux
51
Q

H. pylori associated diseases

A

chronic gastritis
peptic ulcer
gastric carcinoma
gastric MALT lymphoma

52
Q

pathogenesis of H. pylori

A
  • colonisation damages epithelial and endothelial cells
  • bacterial platelet-activating factor → thrombotic occlusion of capillaries
    — produce urease: convert endogenous urea into free ammonia
    — produce peptidase: break down glycoproteins in gastric mucus
    — produce phospholipase: damage epithelial cells → may release bioactive leukotrienes
  • attract neutrophils, while releasing myeloperoxidase
  • other antigens attract inflammatory cells → inflammation makes mucosa more susceptible to acid injury
  • damaged mucosa more permeable → leakage of tissue nutrients → sustain bacteria
53
Q

causes of peptic ulcer

A

H. pylori
smoking, alcohol
drugs: anti inflammatory and analgesics

54
Q

complications of peptic ulcer

A
  • bleeding: ulcer extended deeper into lining damages larger blood vessels
  • perforation: leakage of GIT contents into abdominal cavity → inflammation & infection
  • obstruction: oedema → obstruct pyloric canal/duodenum
  • malignancy: adenocarcinoma
55
Q

liver failure complications / clinical manifestations

A
  • coagulapathy → easy bruising
  • hepatic encephalopathy →impaired hepatic metabolism
  • Cholestasis → jaundice
  • portal hypertension → ascites, splenomegaly
56
Q

cirrhosis
- what?
- causes
- histo

A

scarring/fibrosis of liver

causes:
- viral hepatitis
- DILI
- alcohol liver disease
- bile duct obstruction

histo:
- diffuse transformation of liver to regenerative parenchymal nodules
- surrounded by fibrous bands
- surrounded by variable degree of vascular shunting

57
Q

pathogenesis of portal hypertension
(how cirrhosis → portal hypertension)

A
  1. increased resistance to portal flow
    - vasoconstriction by vascular smooth muscles & myofibroblasts
    - scarring/parenchymal nodules → disrupt blood flow
    - sinusoidal remodelling & arterial-portal shunt (intrahepatic shunt)
  2. increased portal venous flow
    - due to hyperdynanamic circulation
    - arterial vasodilation of splanchnic circulation (blood flow to abdominal GI organs)
58
Q

consequences of portal hypertension

A
  • ascites: increased pressure in peritoneal capillaries → fluid accumulation in peritoneal cavity → abdominal distension
  • portosystemic venous shunts (varices) → bleeding
  • congestive splenomegaly: back flow of blood into spleen → enlarge spleen
  • hepatic encephalopathy: impaired metabolism → shunting of ammonia from GIT into circulation → ammonia alter mental state → asterixis, coma
59
Q

viral hepatitis caused by

A

HEP A/B/C/D/E, EBV, CMV
- Acute liver failure w submassive/
massive hepatic necrosis

(usually Hep A/B/D, in pregnancy Hep E)
- May progress to cirrhosis

(usually Hep B/C)

60
Q

Symptoms of Acute Hepatitis

A
  • Jaundice, dark-coloured urine
  • Fever, fatigue, poor appetite
  • Nausea, vomiting, abdominal pain
61
Q

Fatty Liver Disease Causes

A
  • Diabetes, obesity, starvation
  • Hypoxia
  • Alcoholism
62
Q

consequences of alcoholic liver disease

A
  • Steatosis: accumulation of fat within liver
  • Alcoholic hepatitis: inflammation due to fatty change
  • Steatofibrosis
  • May lead to cirrhosis (10-15%) => HCC (1-6%)
63
Q

pathogenesis of NAFLD
non-alcoholic fatty liver disease

A
  • insulin resistance → dysfunctional lipid metabolism
  • increased production of pro inflammatory cytokines
  • fat laden cells sensitive to peroxidase products → oxidative injury → liver cell necrosis
64
Q

risk factors for HCC

A
  • viral infection: HEP B/C
  • toxin: aflatoxin from Aspergillus flavus
  • metabolic diseases
    NAFLD
65
Q

hep b & c transmission via

A
  • unprotected sex with infected
  • needle prick injury / sharing needles

b: perinatal (transplacentally)
c: haemodialysis without infection control & organ transplant

66
Q

histo for HCC

A
  • trabecular (sinusoidal), pseudoacinar & compact growth patterns
  • polygonal cells with, eosinophilic cytoplasm and distance round nucleus
  • lack portal tracts, Kupffer cells and cohesive connective tissue framework
67
Q

atelectasis

A

collapse of lung - inadequate expansion of lung

68
Q

pneumonia

A

infective inflammation & consolidation of lung
- neutrophils in airspaces

69
Q

risk factors of TB

A
  • chronic lung disease
  • HIV, AIDS, acute renal failure, disease
  • alcoholism, malnutrition
70
Q

gross features / histo for TB

A
  • caseous necrosis → cavitation
  • surrounding fibrosis
71
Q

tuberculosis

A

chronic pneumonia
- communicable, granulomatous & caused by Mycobacterium TB

72
Q

pneumonitis

A

inflammation dominated by interstitial inflammation

73
Q

osteoarthritis
- what
- causes
- gross features/histo

A

chronic progressive degradation of articular cartilage

caused by wear and tear
- genetic abnormalities: familial mutation of type II collagen COL2A1

gross features:
- destruction of articular cartilage → narrowed joint space
- eburnation: loss of cartilage with smooth polished surface
- subchondral cyst formation
- osteophytes: peripheral growth of bone & cartilage
- reactive thickening of synovium

74
Q

rheumatoid arthritis
- what
- causes
- gross features

A

systemic, chronic inflammatory autoimmune disease

causes:
- genetic predisposition (HLA-DR4)
- autoantibodies against cyclic citrullinated peptides (CCPs)

Gross features:
- synovial inflammation - swelling
- pannus formation - hypertrophied synovium & vascular granulation tissue
- destruction of adj bone (due to pannus)
- formation of rheumatoid nodules: granuloma w central zone of fibrinoid necrosis

75
Q

pathogenesis of osteomyelitis

A
  • bacterial proliferation in bone → acute inflammation & bone necrosis
  • bacterial inflammation spread within bone shaft, haversian system & periosteum
  • inflammation within periosteum → sizeable subperiosteal abscess “lifting” periosteum → impair blood supply → cause suppurative injury & further segmental sequestrum
  • rupture of periosteum → abscess in surrounding soft tissue → form draining sinus
76
Q

sequelae of osteomyelitis

A
  • acute OM to chronic OM
  • proliferative periostitis & involucrum
  • pathologic fracture with deformities
  • spread of inflammation/infection elsewhere
  • bone abscess including Brodie’s abscess
  • secondary amyloidosis (chronic OM)
77
Q

gout

A

deposition of urate crystals & increased serum uric acid

78
Q

osteosarcoma

A

produces malignant osteoid
- histo: cytological atypia

79
Q

Ewing sarcoma

A

malignant
NO production of malignant osteoid
translocation of t(11,22)

80
Q

chondrosarcoma

A

production of malignant cartilage
histo: cartilage matrix permeates/invades bone, marrow, soft tissue

81
Q

chondroma

A

benign cartilage

82
Q

osteochondroma

A

contain benign cartilage and bone

83
Q

giant cell tumour

A

benign, epiphyseal-metaphyseal region
- abundant giant cell tumour (osteoclastic type)

84
Q

fibro-osseous tumours
- type n comparison

A

Fibrous Dysplasia (FD) & Ossifying Fibroma (OF)

both: benign bone tumour; contains fibrous tissue & immature bone; same histo

OF vs FD
- FD has GNAS1 mutation
- radiology: OF more circumscribed
- OF higher potential of recurrence

85
Q

clinical manifestations of increase inter cranial pressure (ICP)

A
  • Papilledema (swelling of optic discs)
  • cerebralherniation
  • headache, nausea/vomiting
  • macroencephaly
  • altered mental status
  • crushing triad: bradycardia, hypertension, repsiratory depression
86
Q

pathogenesis of subdural haemorrhage

A

tearing of BRIDGING VEINS in subdural space → extravasation of venous blood
- slow progressive neurological deterioration

87
Q

pathogenesis of subarachnoid haemorrhage

A

increase bp / trauma / spontaneous → rupture of BERRY ANEURYSM

88
Q

pathogenesis of epidural haemorrhage

A

temporal skull bone fracture / trauma → laceration of MMA → extravasation of arterial blood

lucid for 2-3 hours → lose consciousness

89
Q

intracerebral/intraparenchymal haemorrhage

A

hypertension → damage blood vessels → formation of micro-aneurysms

symptoms: headache, nausea, coma, fever, vomiting

if rupture → bleed within parenchyma → brain herniation → death

90
Q

cells of innate and adaptive immune system

A

innate: macrophage, NK cells
adaptive: cell-mediated (T-cells), humoral (B cells & CD4 T cells)

91
Q

alzheimer disease
- region affected, protein inclusions

A
  • brain volume loss
  • affects CEREBRAL CORTEX
  • formation of protein inclusions
    —- extracellular fibrillar Aβ plaques (beta-amyloid)
    —- Intracellular neurofibrillary Tau tangles (Tau protein)
92
Q

parkinson disease
- region affected, protein inclusions

A
  • basal ganglia & brainstem
  • degeneration of dopinergic neuron
  • eosinophilic inclusions (Lewy bodies)
  • proteins: α-Synuclein
93
Q

hypertrophy - physiological causes

A
  • sex organs - testosterone & oestrogen during puberty
  • cardiac muscles - sustained high outflow (athletes)
  • uterine muscles - oestrogen during puberty
  • breast tissue - oestrogen & prolactin for lactation
  • skeletal muscles - exercise
94
Q

hypertrophy - pathological

A
  • LV cardiac muscle - increased outflow pressure (systemic hypertension, aortic valve disease)
  • RV cardiac muscle - increased outflow pressure (pulmonary hypertension, pulmonary valve disease)
    arterial smooth muscle - hypertension
95
Q

hyperplasia - physiological

A
  • breast tissue - during puberty, pregnancy & lactations
  • thyroid - increased metabolic demand during puberty & pregnancy
  • stromal cells in endmetrium: oestrogen during pregnancy
  • RBC precursors in bone marrow - erythropoietin at high altitudes
96
Q

hyperplasia - pathological

A
  • thyroid - graves (autoantibodies effect to TSH receptors
  • stromal cells in endometrium - may lead to endometrial carcinoma
  • skin - persistent trauma (eg corns on feet)
  • parathyroid gland: hypocalcemia
  • prostate gland
97
Q

metaplasia

A

ciliated pseudostratified columnar → squamous
- respiratory tract of smokers
- chronic bronchitis

stratified squamous → simple columnar
- barrett’s oesophagus, gastro-oesophageal reflux

simple columnar → intestinal
- chronic gastritis
- H. pylori in stomach

98
Q

causes of acute inflammation

A
  • infection
  • physical agent: mechanical, heat/cold, ionising radiation
  • chemical agent
  • ischaemia
  • immunological reaction

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