pathophysiology all of them Flashcards

1
Q

cirrhosis

A

liver injury causes cell necrosis and apoptosis
releases cell contents
activates stellate cells and macrophages
phagocytoses apoptotic cells
secretes TGF beta and
stellate become myofibriblasts and proliferate
produce collagen= fibrosis
myofibriblasts and macrophages inhibit MMP so continued scarrinh
cirrhosis

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2
Q

meningitis

A

pathogens enter haemogenous route and spread through bloodstream or nearby infection
bind to endothelial cells and cause cleavage
bacteria able to bind to non-ciliated epithelium via pili and adhesins
trojan horse strategy allows phagocyters to multiply and travel across the BBB
bacterial cell lysis releases PAMP’s and binds to macrophages via PRR and produces pro-inflammatory cytokines
increased inflammation the BBB becomes more permeable and polymorphonuclear granulocytes recruited into the CSF
plasma also enters
increrases cerebral edema and increased intracranial pressure
DAMP production due to borken down endothelial cells= lypoperfusion
increased intracranial presusrer causes brain damage

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3
Q

trojan horse strategy

A

infeciton of phagocytes
pathogen manipulates phagocyte to move to the BBB and suppresses phagocyte activation so it can circualte normally
binds to luminal side of capillaries
crosses BBB
bacteria exits trojan horse to infect neural structures

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4
Q

n. men virulence

A

polysaccharide capsule
LOS endotoxins
type 4 pilus
IgA protease

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5
Q

NMEC virulence

A

K1 capsuel
cytotoxic necrotising capsule
CD48 cells
OmPA adhesion IbeA

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6
Q

alzheimers

A

plaques= amyloid precursor protein, helps neurosn grow and repair, broken down by alpha and gamma secretase enzymes= soluble and recycled but in alzheimers beta and gamma so is insouble
builds up between neurons= inflammation and damage to cholinergic neurons

tangles= cytoskeleton= mictortubules and tau protein holds them together and protein kinase phosphorylates so aggregates= poor signallin

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7
Q

osteoarthritis

A

abnormal stress levels activate chondrocytes in the cartilage leading to proliferation into clusters and MMP’s secreted
MMP’s and pro-inflammatory cytokines cleave aggregan and degrade type 2 cartilage= loss of ECM
cartilage fibirllation
balance tipped so cartilage degraded
no response so no repair
DAMPs cause inflammation causing synovitits
subchondral bone is exposed so increased stress as articulating without cartilage
bone remodelling= osteophytes and subchondral cysts as trapped synovial fluid

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8
Q

DMD

A

x linked recessive
Xp21 mutation in dystrophin
out of frame deletion of exon 52
muscle becomes fibrosed and replaced by fat, 79 exons

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9
Q

bmd

A

inframe mutation
missense
protein function but less expression of the dystrophin gene

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10
Q

menstrual cycle

A

menses: endometrium stratum compactum and spongiosum shed= bleeding
follicular: increased oestrogen so endometrium thickens and proliferates, increased FSH for 15 to 20 follicle maturation
ovulation: increased LH, egg released
luteal: increased progesterone from corpus luteum, prevents porliferatyion and causes thickening of epithelium and endothelium to differentiate and start decidualisation, if no fertilisation then decreased progesterone and oestrogen

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11
Q

puberty precursor

A

in childhood regulatory synpases sent to the GnRH hormones so no production
in puberty leptin binds to LepR activates Kiss1 neurones which synapse with GnRH producing hormones
signals to AP to produce FSH and LH to increase sex steroids

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12
Q

how does a pregnancy test work

A

urine on sample that contains hcg
hcg binds to mobilised antibodies with enzyme attached
immobilised antibodiesin the test zone bind to hcg
enzyme on first antibody changes colour of the line
free antibodies bind to immobilised antibody in the control region= line appeared if positive

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13
Q

sickle cell anaemia

A

point mutation
replace A with T
rna converts GUG to GAG
Val instead of Glu
different 1,2,3,4 proteins
mutation of Hbb gene coding for Hb
recessive

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14
Q

physiological stages of birth

A

oestrogen increases oxytocin receptor on lining of smooth muscle of uterus and regulates progesteroen
progesterone relaxes smooth muscle and prevents contraction
foetal stress= ACTH from AP and stimulates cortisol reelase from adrenal gland
decreased progesterone andoestrogen
increased prostaglandins
prostaglandin= smooth muscle of uterus will contract and stimulate sensory nerve fibres
stimulates oxytocin release from PP
oxytocin= contraction of smooth muscle and increased prostaglandin= positive feedback

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15
Q

influenza

A

virus enters cells
binds onto respiratory epithelium via hemagglutinin spikes and fuses with the membrane
endocytosed into vacuole and uncoated to release 8 nucleocapsids into the cytoplasm
transported to the nucleus where negative sense to postive sense RNA
transcribe viral proteins for capsid and spike
positive strand synthesis= glycoproteins which are inserted into the host membrane
positive to negative = nucleocapsid and transported out of the cell membrane as adheres to sialic acid and buds off as neuraminidaase cleaves it

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16
Q

hepB

A

entry via NCPT receptor
viruse uncoated and releases rCDNA into nucleus
protein free rCDNA to ccDNA to mRNA transcription
leaves nucleus
encapsidisation
reverse transcriptase converts negative sense to positive sense
viral secretion

17
Q

COVID

A

spike porteins bind to ACE2
s glycoproteins cleaved between S1 and 2 domain by enzymes= viral fusion and RNA release
via endocytosis/ pores RNA enters the cytoplasm
uncoating and ssRNA reelased into the cytosol
viral protein produced
glycoproteins processes in the golgi
viral proteins released via vescile exocytosis