pathophy Flashcards
testicular torsion
abnormal attachment of testes dt redundant tunica vaginalis – excessive mobility – twisting of spermatic cord – decreased blood supply, venous congestion – ischemia, necrosis
inguinal hernia incarceration
pressure on herniated viscera causes impaired lymphatic and venous drainage – swelling, compression – decreased blood supply – ischemia, necrosis
congenital inguinal hernia
patent processus vaginalis causes weakness in the abdominal wall musculature, leading to herniation
undescended testis
- hormonal imbalance (insulin-like factor 3, testosterone)
- failure of gubernaculm to guide descent
- failure of processus vaginalis to involute
hydrocele
accumulation of fluid in tunica vaginalis dt defect in procesus vaginalis OR
acquired dt inflammatory conditions (trauma, torsion, epididymitis)
Classic CAH
deficiency of 21-hydroxylase - substrate in synthesis of aldosterone and cortisol, shunting 17-hydroxyprogestrone to androgen synthesis
CDH
- defect between the abdominal and thoracic cavities with or without herniation of bowel loops into chest cavity
- Herniated abdominal contents compress the lungs and result in pulmonary hypoplasia
STI
in females
increase in estrogen leads to changes in the vaginal epithelium, leading to decreased pH and increased susceptibility to organisms
T1DM, DKA
- autoimmune damage to pancreatic B cells leads to low or absent endogenous insulin
- decreased gluc utilization in ms and fat; increased production in liver
- causing hyperglycemia which causes osmotic diuresis and ketone body formation
acute pancreatitis
initial insult (injury, infection) causes increase in proenzymes leading to pancreatic autodigestion
acute appendicitis
phlegmon or lymphoid hyperplasia causes obstruction, leading to congestion, edema, ischemia, and necrosis
necrotizing enterocolitis
dysbiosis due to prematurity, early enteral nutrition causes bacterial overgrowth, leading to inflammation, intestinal ischemia and necrosis
pertussis
oragnism and pertussis toxin induces inflammatory response – inflammation, epithelial damage – respiratory sx
kawasaki
acute systemic vasculitis of medium-sized vessels
TB meningitis
TB bacilli enters CNS, forms casseous lesion, releases gelatinous exudates, causing inflammation, obstruction, infarction, leading to CNS dysfunction
PSGN
- molecular mimicry between antibodies elicited by strep antigen and gbm and
- direct deposition of strep ag in glomeruli causes complement activation and immune complex formation
HUS
infection triggers endothelial injury, leading to platelet aggregation; endothelial injury causes destruction of RBCs and glomerular thrombosis – decreased glomerular filtration
HSP/ IgA Vasculitis
IgA deposition in small vessels causes necrotizing vasculitis in end organs such as kidneys
SLE
autoantibodies against self antigens form immune complexes and deposit in end-organs, causing inflammation and tissue damage
Septic arthritis
hematogenous seeding of synovial space
Intussusception
intussusceptum telescopes into intussuscipiens, pulling its mesentery along and causing venous congestion, edema, and bleeding from mucosa, causing bloody stool
RDS
surfactant deficiency and/or prematurity causes increased surface tension and alveolar collapse, leading to hypoxia and respiratory distress
SSPE
altered measles virus seeds in CNS and reactivates 7-13 years after initial infection, causing behavioral changes, neuro sx
EBV
virus enters respi epith, spreads to salivary glands, travels to reticuloendothelial system - causing lymphadenopathy, hepatosplenomegaly
Dengue
virus enters bloodstream via bite from mosquito vector, toxins trigger inflammatory cytokines and complement cascade, causing increase vascular permeability
leptospirosis
leptospira enter body via mucous membranes, break in the skin, or ingestion; cause endothelial damage to small bv and end-organ ischemia
bronchiolitis
viral infection causes inflammation and obstruction of small airways with edema, mucus, and cellular debris
Acute bacterial meningitis
bacterial colonization of nasopharynx and subsequent bacteremia causes organism to cross BBB and enter CNS, causing inflammation, injury and meningial irritation
Japanese encephalitis
virus enters CNS and causes direct neurotoxic effects
COVID
Viral spike protein binds to Angiotensin Converting Enzyme 2 (ACE-2) receptors in airway epithelial and endothelial cells which:
1. Reduces ACE2 expression in the lungs resulting in acute lung injury,
2. Causes dysregulation of the reninangiotensin system resulting in hemodynamic instability
Malaria
plasmodium enters bloodstream, enters liver and releases merozoites
TTN
- delayed fluid resorption dt lack of maternal squeeze and catecholamine surge
- increased lung compliance and resistance
- impaired gas exchange, acidosis
MAS
- partial airway obstruction leading to ball-valve effect which allows inflow of air but causes air trapping
- inhibition of surfactant and inflammation and obstruction of small airways
- all leading to hypoxemia, hypercapnia, acidosis
Hirschsprung
absence of ganglion cells in mucosa and submucosa causing inadequate relaxation of bowel wall
Diphtheria
diphtheria exotoxin inhibits protein synthesis, causes local tissue necrosis and inflammation → formation of gray-brown, leather-like adherent PSEUDOMEMBRANE
Bronchial asthma
chronic airway inflammation, airway hyperresponsiveness and variable airflow limitation cause respiratory sx (cough, wheezing, DOB)
TOF
anteriorly and superiorly deviated infundibular septum leading to PROV (pulmonary stenosis, RVH, overriding of the aorta, VSD)
ARF
- cytotoxic toxins damage cardiac cells
- cross-reactivity bet GAS epitopes and cardiac cells (molecular mimicry)
- M protein binds to collagen type IV and causes inflammation in cardiac cells
Tet spells
- decrease in SVR (dt crying, feeding, defecatin) leads to increased venous return, and increased R to L shunting
- causes acidosis, hyperpnea, further increase in SVR
pericarditis
fluid within the pericardial layers increases dt infection/inflammation, leading to compression of the chambers and impaired cardiac filling
typhoid
- typhoid toxin penetrates intestinal lumen, causes necrosis of peyers patches, leading to inflammation and gastroenteritis;
- spreads via lymphatics to liver, spleen, BM
tetanus
spores enter via traumatic injury and release tetanospasmin which inhibits release of glutamate and gaba in NMJ, causing sustained maximal contraction and spastic paralysis
botulism
ingested spores produce neurotoxin which irreversibly block presynaptic release of acetylcholine, inhibiting NM transmission, causing muscle paralysis
rabies
virus enters the body via a bite or scratch from infected animal, replicates in ms or skin then enters CNS via retrograde axonal transport, infects brainstem and spinal cord, causing CNS dysfunction
poliomyelitis
virus enters body via feco-oral route, replicates in small intestine, seeds in CNS
- causes inflammation, edema, neuronal damage, causing flaccid paralysis
pulmonary TB
- tubercle bacilli enter the body via inhaled respiratory droplets, cause local inflammatory reaction
- macrophages phagocytose bacteria, tubercle bacilli multiply within macrophage and form casseous lesions which spread via lymphatics
- casseous foci in lungs cause inflammation and obstruction, leading to respiratory sx
anaphylaxis
IgE and other immunnologic mediators, cause mast cell and basophil degranulation
- causing release of histamine, prostaglandin, and other mediators
- cause cutaneous, respi, GI manifestations
osteomyelitis
- low velocity blood flow in metaphysis leads to bacterial invasion
- causing inflammation, proteolysis and osteolysis
JIA
- immunologic susceptibility triggered by environmental factor (infection) causes synovitis of peripheral joints with swelling and effusion
Myasthenia gravis
- antibodies to Ach receptors lead to impaired NM transmission, causing asymmetric descending muscle weakness
Rh incompatibility
- mother with Rh- blood develops antibodies after exposure to Rh+ blood from delivery of 1st bb
- maternal antibodies to Rh+ blood are passed on via placenta during succeeding pregnancies
- causes RBC destruction in infant, causing hemolysis and jaundice
Breastfeeding jaundice
- decreased milk production leads to dehydration and hemoconcentration of bilirubin, causing less BM and increased enterohepatic circulation
Breastmilk jaundice
- beta glucoronidase in breastmilk deconjugates bilirubin and leads to increased enterohepatic circulation
ABO incompatibility
- maternal antibodies against ABO factors in fetus form antigen-antibody complexes, causing hemolysis and jaundice
G6PD
- glucose 6 phosphate dehydrogenase catalyzes initial step in HMP which protects RBC from oxidative injury
- deficiency of G6PD makes RBCs more prone to oxidative stress and injury, leading to hemolysis
Biliary atresia
- failure of dev or progressive injury of portion or entire biliary system, causing obstructive jaundice
Functional constipation
- children develop intentional or subconscious withholding of BM due to a social stressor, toilet training, school entry, or change in diet
- stool becomes firm and difficult to pass and passage of BM becomes painful
- causing voluntary withholding of stool to avoid discomfort
AOM
- viral URTI causes inflammation of respiratory mucosa
- increased secretions causes obstruction bacterial overgrowth
- infection and inflammation of middle ear
AOE
- irritation from excess moisture leads to inflammation and increased secretions
pnemothorax
- loss of negative pressure in intrapleural space
- causes lung collapse
- leading to hypoventilation and hypoxemia
