pathology Flashcards
pathogenesis of atherosclerosis
- 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
MI – how MI leads to pulmonary & ankle oedema
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
complications of MI
Myocardial rupture
Congestive heart failure
Fibrosis
Aneurysm
Thrombus
Pericarditis
Ruptured papillary muscle
Arrhythmia
Contractile dysfunciton
modifiable risk factors of MI
smoking
hyperlipidemia
hypertension
diabetes
non-modifiable risk factors of MI
age
gender
family history
genetics
infective endocarditis (what? cause? symptoms?)
infection of valves
- acute: S aureus
- subacute: Viridans strep
form vegetation → destroy tissues
symptoms: fever, chills, heart murmur
rheumatic heart disease
abnormal immune response (to group A Strep Pharyngitis)
- inflammation & damage to heart valves → stenosis and regurgitation
causes of hyperthyroidism
primary: Graves, toxic multi nodular goitre, toxic neoplasm
secondary: pituitary hyperfunction
causes of hypothyroidism
primary: hashimoto (most common), iatrogenic
secondary: pituitary failure
cretinism (congenital in children) – dietary iodine deficiency
symptoms + biochemical signs of hyperthyroidism
weight loss
hot - heat intolerance
oligomenorrhoea (infrequent period)
diarrhoea
irritable mental state
increased appetites
high T3, T4
low TSH
symptoms + biochemical signs of hypothyroidism
weight gain
cold intolerance
menorrhagia (heavy period)
constipation
mental slowness
decreased appetite
low T3, T4
high TSH (primary), low TSH (secondary)
pathogenesis of graves
- autoantibodies bind & activate TSH receptor
- release of T3, T4
- increase cellularity & hyperplasia of gland
gross features of graves
- diffuse enlargement
- red meaty cut surface
- smooth & soft gland, intact capsule
histology:
- follicular cells tall, columnar, crowded – pseudopapillae
- inflammatory cells
gross features of hashimoto
- pale
- enlarged
histology:
- lymphoid follicles
- hurthle cell changes
which thyroid carcinoma metastasise via bloodstream
follicular carcinoma
which thyroid carcinoma metastasise via lymphatics (LN)
papillary carcinoma
medullary carcinoma associated with??
MEN (multiple endocrine neoplasia)
- younger patient
diagnosis for single thyroid nodule
follicular adenoma
follicular carcinoma
papillary carcinoma
anaplastic carcinoma
medullary carcinoma
features of papillary carcinoma
- nuclear features: finely dispersed chromatin, nuclear grooves, pseudo inclusions
- papillae with fibrovascular cores
- psammoma bodies
MEN 1 associated with which gene mutation
MENIN gene mutation
MEN 2 associated with which gene mutation
RET gene mutation
MEN 1 clinical feature
PHAIG
prolactinoma - excessive breast milk production
hyperparathyroidism - hypercalcemia
adrenal adenoma – cushing syndrome
insulinoma
gastrinoma - gastric ulceration
MEN 2B clinical feature
- mucosal neuroma syndrome (growth around nerves of mucous membranes)
- marfanoid syndrome (long limbs, loose joints, curved spine)
role of PTH
increase Ca levels by
- ↑ bone resorption by osteoblasts
- ↑ renal tubular absorption
- ↑ intestinal absorption (mediated by Vit D, PTH ↑ its synthesis)
causes of hyperparathyroidism
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)
effects/consequences of parathyroidism
- renal & urinary calculi
- osteitis fibrous cystica
- hypertension
- pancreatitis
- peptic ulcer
- metastatic calcification
causes of hypoparathyroidism
iatrogenic (surgery)
autoimmune
causes of adrenal hyperfunction
primary
- adrenal adenoma/carcinoma
- adrenal hyperplasia
secondary
- pituitary adenoma
Cushing syndrome clinical features
cushing is due to increase in cortisol
- adrenal tumour/hyperplasia
- moon face, buffalo hump, obesity
- hyperglycaemia
- hypertension
- osteoporosis
- thin wrinkled skin, abdominal striae
- muscle weakness
- emotional disturbance
- skin ulcers (poor wound healing)
- amenorrhea
causes of adrenal hypofunction
primary
- iatrogenic (surgery)
- autoimmune
- haemorrhage (blood vessels in adrenal gland rupture)
- infections: TB, histoplasmosis
- metastatic tumours
secondary
- pituitary disease
effects of adrenal hypofunction
- weight loss
- muscle weakness
- low BP
- poor immune response
polycythaemia
too much RBCs
- associated with hypoxia – living at high altitudes
causes of anaemia
too few RBC
- decrease production: iron/B12/folate deficiencies
- bleeding
- increased destruction: Hb defects (sickle cell / thalassaemia), enzyme defects (G6PD)
symptoms of anaemia
pallor
weakness
dizziness/syncope
palpitation, chest pain, shortness of breath
leukocytosis – following associated with what
- neutrophilia
- eosinophilia
- monocytosis
- lymphocytosis
- neutrophilia: infection, tissue necrosis
- eosinophilia: allergies, parasitic infection
- monocytosis: chronic infections (eg. TB), autoimmune disease
- lymphocytosis: viral infections, TB
thrombocytosis – what? and causes
too many platelets
primary: neoplastic
secondary:
- hemorrhage
- splenectomy
- infections
- inflammatory conditions (autoimmune disease)
effects of thrombocytosis
thrombosis
bruising
bleeding
thrombocytopenia
too few platelets
caused by
- bone marrow damage (Chemo/radiotherapy),
- autoimmune disease
- hypersplenism (splenomegaly)
- increased consumption (shock, burns, sepsis)
effects of thrombocytopenia
- petechiae
- bruising
- bleeding (nose bleed; internal bleeds)
- prolonged bleeding