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30 Cards in this Set

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The beta cells of the pancreas are good sensors of plasma concentrations of glucose. How is this achieved?
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]
Insulin secretion from beta cells in 6 steps
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
Endocrine cells take up approx how much of the pancreas cell mass?
2%
Describe insulin synthesis
it's a polypeptide hormone. Preproinsulin, proinsulin (A and B chain linked by disulphide bonds, C peptide joins them), cleavage leads to insulin
Cell types in the islets of langerhan. Relative abundance and what they secrete
Beta cells 60% insulin
alpha cells 25% glucagon
delta cells somatostatin
The insulin receptor is what kind of a receptor?
tyrosine kinase
Define shock, and the formula for a good indicator
Shock = multisystem hypoperfusion. HR > systolic BP is a useful indicator
An anaphylactic shock is what type of shock? General mechs of this type of shock?
Distributive, other eg = septic shock. Systemic vasodilation leads to decr BP, "warm" shock
3 main types of shock
Hypovolaemic, cardiogenic, distributive (others = neurogenic [resulting in vasodilation], obstructive [obstruction of bld flow to heart or lungs])
Shock - Signs and symptoms
stage 1 (compensated): pallor, slight anxiety
Uncompensated = ↑ HR, ↓ BP, ↓ pulse pressure. ↑ RR, sweating, cold clammy skin, altered mental state, ↓ cap return, ↓ urine output
Isotype of Ig predominant in response to secondary infection
IgG
Isotype of Ig predominant in response to a primary infection
IgM
Which Ig isotype works mostly by neutralising ag in the GIT and secretory ducts?
IgA
Egs of primary immunodeficiency
Chronic Granulomatous Disease (neutrophil can’t produce superoxides)
Hyper IgM Syndrome (no class switching)
DiGeorge syndrome (thymic aplasia → T cell deficiency)
Secondary immunodeficiency can be caused by?
HIV infection → AIDS, malnutrition
Define failure to thrive
Bottom 3rd-5th percentile on 2 or more occasions

Drop in 2 major percentiles in 6 mths
Differences between thick and thin skin
Thick skin: hairless, palms and feet, thicker epidermis, has stratum lucidum; interface between dermis and epidermis has ridges = finger prints
Layers of the epidermis
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)
How do keratinocytes come to possess melanosomes?
Melanocytes found between cells of stratum germinativum synthesise melanin. Melanosomes are passed to keratinocytes from the melanocyte dendrites.
Two layers of dermis
Papillary (superficial)

Reticular (the main bulk)
Pathogenesis of inflammatory acne vulgaris (4 elements)
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
What is a sebaceous follicle?
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
Sebum is…?
Lipid based secretion, contains triglyceride, cholesterol, protein, electrolyte. Maintains hydration of epidermis and hair, antibacterial. Secreted by sebaceous glands and follicles.
What’s wrong with the statement “acnes vulgaris is an infection”?
It’s not. it’s an inflammation.
Define diarrhoea
↑ volume, ↑ frequency and/or Δ consistency
Mechanisms of diarrhoea
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
Digestion of carbohydrates
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
Digestion of proteins
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
Digestion of lipids
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.
Most absorption of nutrients occurs in which region of the small intestine?
Jejunum
Duodenum = some lipid and aa; Ileum = bile salt and vit B12, the only site where these can be absorbed