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30 Cards in this Set
- Front
- Back
The beta cells of the pancreas are good sensors of plasma concentrations of glucose. How is this achieved?
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GLUT 2 and glucokinase both have much higher Km values (ie lower affinity) than ur average GLUT1,3 and hexokinase. This means they are sensitive to a wider range of change in [glucose]
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Insulin secretion from beta cells in 6 steps
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1. glucose enters GLUT 2
2. incr glycolysis = incr ATP 3. inhibition of ATP-sensitive K channel 4. depolarisation 5. v-gated Ca ch Open 6. exocytosis |
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Endocrine cells take up approx how much of the pancreas cell mass?
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2%
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Describe insulin synthesis
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it's a polypeptide hormone. Preproinsulin, proinsulin (A and B chain linked by disulphide bonds, C peptide joins them), cleavage leads to insulin
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Cell types in the islets of langerhan. Relative abundance and what they secrete
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Beta cells 60% insulin
alpha cells 25% glucagon delta cells somatostatin |
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The insulin receptor is what kind of a receptor?
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tyrosine kinase
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Define shock, and the formula for a good indicator
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Shock = multisystem hypoperfusion. HR > systolic BP is a useful indicator
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An anaphylactic shock is what type of shock? General mechs of this type of shock?
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Distributive, other eg = septic shock. Systemic vasodilation leads to decr BP, "warm" shock
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3 main types of shock
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Hypovolaemic, cardiogenic, distributive (others = neurogenic [resulting in vasodilation], obstructive [obstruction of bld flow to heart or lungs])
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Shock - Signs and symptoms
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stage 1 (compensated): pallor, slight anxiety
Uncompensated = ↑ HR, ↓ BP, ↓ pulse pressure. ↑ RR, sweating, cold clammy skin, altered mental state, ↓ cap return, ↓ urine output |
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Isotype of Ig predominant in response to secondary infection
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IgG
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Isotype of Ig predominant in response to a primary infection
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IgM
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Which Ig isotype works mostly by neutralising ag in the GIT and secretory ducts?
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IgA
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Egs of primary immunodeficiency
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Chronic Granulomatous Disease (neutrophil can’t produce superoxides)
Hyper IgM Syndrome (no class switching) DiGeorge syndrome (thymic aplasia → T cell deficiency) |
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Secondary immunodeficiency can be caused by?
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HIV infection → AIDS, malnutrition
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Define failure to thrive
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Bottom 3rd-5th percentile on 2 or more occasions
Drop in 2 major percentiles in 6 mths |
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Differences between thick and thin skin
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Thick skin: hairless, palms and feet, thicker epidermis, has stratum lucidum; interface between dermis and epidermis has ridges = finger prints
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Layers of the epidermis
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Stratum germinativum/basale (single layer, stem cells)
Stratum spinosum (start to accumulate keratin and flatten/elongate) Stratum granulosum (keratohyalin granules – densely staining; nuclei starts to degenerate) Stratum lucidum (thick skin only) Stratum corneum (dead anuclear cells packed with keratin) |
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How do keratinocytes come to possess melanosomes?
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Melanocytes found between cells of stratum germinativum synthesise melanin. Melanosomes are passed to keratinocytes from the melanocyte dendrites.
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Two layers of dermis
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Papillary (superficial)
Reticular (the main bulk) |
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Pathogenesis of inflammatory acne vulgaris (4 elements)
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1. Comedogenesis: abnormal keratinisation of sebaceous follicle epithelium → plugged pilosebaceous unit = white heads (closed comedone) or black heads (opened)
2. ↑ Sebum production (eg. due to androgens in puberty) 3. Proliferation of P. acnes 4. Inflammatory response, can be exacerbated by follicular wall rupture → spillage of contents into dermis |
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What is a sebaceous follicle?
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Pilosebaceous unit
– secretes sebum direct to skin surface - produce fine vellus hair - large sebaceous gland - widely dilated follicular canal (stratified squamous keratinising epithelium) - site of Acne! v.s. sebaceous glands, which secrete sebum into hair follicle |
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Sebum is…?
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Lipid based secretion, contains triglyceride, cholesterol, protein, electrolyte. Maintains hydration of epidermis and hair, antibacterial. Secreted by sebaceous glands and follicles.
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What’s wrong with the statement “acnes vulgaris is an infection”?
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It’s not. it’s an inflammation.
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Define diarrhoea
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↑ volume, ↑ frequency and/or Δ consistency
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Mechanisms of diarrhoea
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MODES
Malabsorption (→ osmotic diarrhoea; eg. vilous atrophy in celiac disease; lack of digestion/impaired enzyme activity) Osmotic: eg. lactose intolerance + above for malabsorption) Deranged motility: increased (→ ↓absorption) or decreased (→ ↑bact growth → bile acid deconjugation → steatorrhoea and diarrhoea) Exudative/inflammatory: damage to mucosa → inflammation → blood, pus, mucus in faeces eg. dysentery, infections (Salmonella, Shigella, Campylobacter) or inflammatory bowel disease) Secretory: abnormal ion transport → increase secretion (eg. cholera) or decreased absorption, or both. No structural damage Mechanisms rarely occur alone |
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Digestion of carbohydrates
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Amylase (salivary and pancreatic) breaks down polysaccharides → di- and trisaccharide arrive at SI → brush border enzymes cleaves → monosaccharide (maltase, lactase, sucrase)
Glucose and galactose enter brush border cell via cotransporter SGLT 1, fructose via facilitated diffusion through GLUT 5 |
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Digestion of proteins
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Stomach: pepsin and HCl
Duodenum: pancreatic enzymes SI: peptidases tethered to brushborder → small peptides and aa transported into epithelial cell. intracell peptidase cleaves small peptide into aa |
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Digestion of lipids
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Lipases (lingual, gastric (min amount)+ PANCREATIC)
Bile salts → emulsification of lipids → ↑ surface area for lipase contact fatty acids, cholesterol and monoglycerides arrive at SI, diffuse into epithelial cells. Made → TAG → chylomicron and transported to lacteal (too big for capillary) → lymph. Small and medium FA → released straight into blood → bind to albumin. |
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Most absorption of nutrients occurs in which region of the small intestine?
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Jejunum
Duodenum = some lipid and aa; Ileum = bile salt and vit B12, the only site where these can be absorbed |