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3rd Year > Cases 15 and 16 > Flashcards

Cases 15 and 16 Flashcards

0
Q

Functions of insulin

A 
Increase glucose uptake
Increase protein synthesis
Increase fat deposition
Increase potassium uptake into cells
Decrease glycogenolysis and gluconeogenesis
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1
Q

Ketone synthesis

A

During fasting or high fat low carb diet
Glucagon/insulin ratio high
Excess acetyl CoA from B oxidation of fatty acids
Converted to ketones in liver mitochondria

And

Oxaloacetate converted to malate and exported from mitochondrion for gluconeogenesis
Less oxaloaxetate in TCA cycle, therefore AcetylCoA levels rise
Excess acetyl CoA converted to ketones in liver mitochondria

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2
Q

Effects of the glucose counter regulatory hormones

A

Glucagon: glycogenolysis and gluconeogenesis
Adrenaline: lipolysis and glycogenolysis
GH: lipolysis and glycogenolysis
Cortisol: proteolysis and gluconeogenesis

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3
Q

Clinical features type 1 diabetes

A 
Usually less than 30 years old
Usually lean
Acute onset
Almostalways symptomatic
Usually unequivocal hyperglycaemia
Insulin necessary for survival
Otherwise healthy
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4
Q

Clinical features type 2 diabetes

A 
Usually older
Overweight or obese
Insidious onset
Often asymptomatic
Not prone to ketosis
Usually controlled with non-insulin therapies
Often have comorbidities
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5
Q

Symptoms of diabetes mellitus

A

Weight loss
Polyuria
Polydipsia
Polyphagia

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6
Q

Complications of diabetes

A

Acute: DKA, HONK

Macrovascular:
CAD
Peripheral vascular disease
Stroke

Microvascular:
Retinopathy
Nephropathy
Neuropathy

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7
Q

What is HbA1c?

A

Haemoglobin with a glucose attached to the N-terminal valine of the beta chain

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8
Q

Factors interfering with HbA1c interpretation

A 
Shortened RBC lifetime:
Haemolytic disease
Sickle cell disease
Pregnancy
Chronic blood loss
Increase RBC lifetime:
Fe deficiency
Pregnancy
Splenectomy
Aplastic anemia

Haemoglobinopathies

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9
Q

Diagnosis of diabetes

A

Fasting glucose >7 mmol/l. (11.1 mmol/l and symptoms of hyperglycaemia

HbA1c >6.5%. (<6%)

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10
Q

Pathogenesis of DKA

A

No insulin

Gluconeogenesis, glycogenolysis
Hyperglycaemia, glycosuria
Osmotic diuresis
Dehydration

Lipolysis
Ketones
Acidosis and vomiting
Dehydration

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11
Q

HONK pathogenesis

A

Hyperglycaemia due to low insulin
Glycosuria causes osmotic diuresis
Dehydration and hyperglycaemia cause increased plasma osmolarity.
Cerebral dehydration, increased viscosity and thrombosis

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12
Q

Mechanism of hypokalaemia in DKA

A

Depletion of glycolytic intermediates causes fewer K+ binding sites
Accumulating H ions displace K from intracellular proteins
Excess plasma K is cleared by the kidneys, giving a high normal level at presentation obscuring profound intracellular depletion

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13
Q

Treatment of DKA

A 
Rehydration, avoid cerebral oedema
Monitor and replace electrolytes (K, Mg and Phosphate)
Insulin until normal pH
(Bicarbonate)
Look for and treat underlying cause
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14
Q

Features of hypoglycaemia

A

Blood glucose <2.2 mmol/l

Neuroglycopaenia: faintness, weakness, headache

Sympathetic stimulation: paplitations, tachycardia, sweating

Changes in behaviour, confusion, seizures, coma

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15
Q

Causes of hypoglycaemia

A

Drugs: insulin, alcohol
Neoplasms: insulinoma, IGF secreting tumours
Liver disease
Endocrine disease: addison’s, GH deficiency
Sepsis

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16
Q

Hypoglycaemia investigations

A 
Insulin
C peptide
Ketones
Cortisol
Growth hormone
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17
Q

Causes of hypoglycaemia in diabetes

A 
Exercise
Missed meals
Innapropriate insulin or secretagogue
Progressive renal failure causing decreased renal insulin clearance
Alcohol
18
Q

Mini ethnography

A 
Ethnic identity
What is at stake
Illness narrative 
Psychosocial stressors
Influence of culture on the clinical relationship
Is this schema useful here?
19
Q

What is kinship?

A

Relationship between entities that share a genealogical background, inclusive of descent and marriage

20
Q

What is stigma?

A

Linking a person to a set of undesirable characteristics that may lead to prejudice and discrimination

21
Q

Critical elements of cultural competency

A

Communication repertoire: build relationships, gather information, manage patients in distress

Situational awareness: patient cues, conecting

Adaptability to different cultural divides

Knowledge of core cultural issues

22
Q

Pancreatic islet cells

A

Alpha: produce glucagon

Beta: insulin

D cells: secrete somatostatin which inhibits insulin and glucagon

23
Q

Stimuli for insulin secretion

A

Hyperglycaemia
Amino acids
Gastrin, secretin
Parasympathetic stimulation

24
Q

Stimuli for glucagon secretion

A

Hypoglycaemia
NE and E
Amino acids

25
Q

Mechanism of insulin secretion

A

Glucose enters beta cell via GLUT 2
Glycolysis and mitochondrial metabolism produce ATP
ATP dependent K channels close causing depolarisation
Ca channels open
Ca induces insulin granule exocytosis

26
Q

Energy balance signals

A

Insulin crosses BBB and binds to insulin receptors in the hypothalamic arcuate nucleus, reducing food intake.

The adipocytokine leptin conveys the status of the peripheral fat stores in a similar fashion. It suppresses appetite, increases energy expenditure and promotes fecundity.

27
Q

Gut satiety peptides

A

GLP-1 is made by L type enterocytes in the ileum. Glucose and FFAs bin to the apical poles of these cells, stimulating GLP release. GLP inhibits gastric secretion, stimulates insulin release and has a small anorexigenic effect.

Oxyntomodulin is released in by the same cells inr esponse to the same stimuli but is potently anorexigenic.

PYY binds to and inhibits NPY producing neurons which normally stimulate appetite

28
Q

Ghrelin

A

Secreted by enteroendocrine cells int he fundus of the stomach. Stimulates orexigenic NPY neurons in the arcuate nucleus. Levels rise with fasting

29
Q

Pathogenesis of primary diabetes

A

Type 1: inheritable with HLA associations. Autoimmune damage to pancreatic beta islet cells following environmental trigger in susceptible individual.

Type 2: obesity,insulin receptor or post-receptor defects

30
Q

Secondary diabetes

A

Endocrinopathies
Gestational diabetes
Drugs
Pancreatic damage

31
Q

Mechanism of diabetic complications

A

Advanced glycation end products lead to inflammatory changes leading to atheroma and thickened BM with increased matrix deposition

Activation of protein kinase C leads to angiogenesis, inflammation

Sorbitol and fructosed decrease myoinositol levels lead to schwann cll and pericyte injury

Increased 02 free radicals

32
Q

Pancreatic polypeptide

A

Secreted by F islet cells
Inhibits somatostatin secretion
Inhibits pancreatic enzyme and and bile release

33
Q

Histology of the adenohypophysis

A

No BBB
Cellular cords surrounding fenestrated capillaries
Acidophils: peptide hormones GH and prolactin
Basophils: glycoproteins. FSH, LH, TSH, ACTH
Chromophobes

34
Q

Blood supply to the pituitary gland

A

The superior hypophysial artery forms the primary capillary plexus in the infundibulum where it collects hypothalamic secretions. E primary plexus is drained by portal veins which go on to form the secondary plexus in the adenohypophysis.

The inferior hypophysial artery supplies the pars nervosa, forming a plexus which collects oxytocin and ADH secretions.

The superior and inferior hypophysial arteries are linked by the trabecular artery

35
Q

What are the secretory granules found in the pars nervosa called?

A

Herring bodies

36
Q

Thyroid hormone synthesis

A

Exocrine phase:
Uptake of iodide by STP driven iodide pump in the basal membrane of follicular cells, concentrating iodide within the cell. Iodide diffuses into the colloid.

Thyroglobulin is synthesised at the rER and Golgi apparatus. Thyroglobulin and thyroid peroxidase are present in the same secretory vesicle. Thyroid peroxidase is activated at the apical membrane and converts iodide to iodine. Iodination of thyroglobulin takes place in the colloidal lumen.

Endocrine phase:
Colloid droplets containing iodinated thryoglobulin are endocytosed by apical pseudopodiaa and guided to a lysosome where proteolytic enzymes cleave thyroglobulin to release T3 and T4.
T3 and T4 are released into the bloodstream across the basal membrane.

37
Q

Distinguishing active and passive thyroid gland on histology

A

Active: columnar follicular epithelium, colloid droplets within follicular cells, large apical pseudopodia and microvilli

Passive: enlarged colloid, cuboidal follicular epithelium

38
Q

Parathyroid gland histology

A

Cord like arrangement of cells surrounding sinusoidal capillaries

Chief cells: secrete PTH, glycogen inclusions may be visible

Oxyphil cells: contain abundant mitochondria. May represent a transitional form of chief cells

39
Q

PTH functions

A

Stimalates bone resorption by stimulating osteoclastogenesis via M-CSF and RANK ligand expression

Acts on the kidney to stimulate Ca reabsorption and stimulates vitamin D release

40
Q

Histology of the adrenal gland

A

Fibrous capsule

Zona glomerulosa: concentrically arranged cells containing a few lipid droplets. Thinnest layer. Aldosterone under angiotensin II control.

Zona fasciculata: polygonal cells arranged in columns separated by capillaries. Vacuolated. Thickest layer. Cortisol under ACTH control

Zona reticularis: darker staining anastamosing cells arranged in a network surrounded by capillaries. Sex steroids under ACTH control

Medulla: epinephrine and norepinephrine secreting cells surrounded by venous sinusoids

41
Q

Mechanisms of action of metformin and sulfonylureas

A

Metformin (biguanide): decreases hepatic gluconeogenesis and enhances peripheral GLUT 4 deployment

Sulfonylureas: insulin secretagogue. Bind to ATP dependent hyperpolarising K channels in beta cells causing increased membrane fusion of insulin vesicles

42
Q

Insulin action on the cell

A

Insulin bands to the alpha subunit of the insulin receptor
This causes a conformational change and phosphorylation of the insulin response substrate IR by protein kinases causing a cascade of cellular responses including GLUT 4 deployment

3rd Year (7 decks)

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