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Year 2 Session 2 > 2100 - Renal > Flashcards

2100 - Renal Flashcards

1
Q

Signalling mechanism of steroids.

A

Intra and extra cellular receptors. Intra (classical genomic signalling): hormone binds to receptor in cytoplasm > nucleus, acts as nuclear transcription factor/genomic receptor, binds to DNA at hormone response elements > gene expression

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2
Q

Examples of steroids and associated organ.

A

Gonads - androgens - sex hormones (progesterone, testosterone and estradiol).
Adrenal cortex - corticosteroids, mineralocorticoids and androgens
Skin - vit D

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3
Q

Steroid production.

A

Enzymatically derived from cholesterol in smooth ER of cells - Steroidogenic pathway

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4
Q

Somatostatin is also…

A

GHIH

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5
Q

Somatotropin is also…

A

Growth hormone

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6
Q

Primary endocrine organs (9)

A

Hypothalamus, pituitary, pineal, thyroid/parathyroid, adrenal glands, pancreas, ovaries, testes, placenta

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7
Q

Secondary endocrine organs (7)

A

Kidney, uterus, liver, stomach, sml intestine, thymus, heart

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8
Q

Pineal gland releases (1)

A

Melatonin

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9
Q

Thyroid/parathyroid release (4)

A

T3, T4, Calcitonin, PTH

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10
Q

Adrenal gland releases (4?)

A

mineralocorticoids (aldosterone), sex hormones (androgens and estrogens), corticosteroids (glucocorticoids-cortisol), catecholamines

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11
Q

Pancreas releases (3)

A

insulin, glucagon, somatostatin (GHIH)

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12
Q

Ovaries release (2)

A

Estrogen, progesterone

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13
Q

Testes release (2)

A

Androgens, estradiol

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14
Q

Placenta releases (1)

A

hCG

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15
Q

Kidney releases (3)

A

Calcitriol (vit D), renin, erythropoietin

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16
Q

Uterus releases (2)

A

Prolactin, relaxin

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17
Q

Liver releases (2)

A

Thrombopoietin, IGF-1

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18
Q

Stomach releases (5)

A

Gastrin, ghrelin, histamine, somatostatin (GHIH), neuropeptide Y

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19
Q

Sml intestine releases (3)

A

CCK, secretin, somatostatin (GHIH)

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20
Q

Thymus produces (1)

A

Thymopoietin

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21
Q

Heart (1)

A

Atrial natriuretic peptide

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22
Q

Steroid transport in blood

A

Bound to globulins (long half life)

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23
Q

Globulins are made in the

A

liver

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24
Q

Hormones are inactive when

A

bound

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25
Q

Steroid properties

A

non-polar - lipophilic, hydrophobic

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26
Q

Peptide hormone production

A

rER and GA (chains of aa, cleaved from pro-hormone to hormone)

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27
Q

Peptide hormone release

A

Vesicles - exocytosis (Ca dependent)

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28
Q

Peptide hormone transport

A

Unbound (active)

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29
Q

Peptide hormone receptors

A

Extracellular: ligand-gated ion channel, enzyme-linked receptor, GPCR

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30
Q

Peptide hormone properties

A

Polar, hydrophilic

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31
Q

Peptide hormone example

A

Insulin (pancreas)

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32
Q

Amine hormone synthesis

A

Derived from amino acids.
Tyrosine > (nor)epinephrine, T3/4
Tryptophan > melatonin, serotonin

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33
Q

Which amine hormones are steroid-like

A

T3, T4

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34
Q

Which amine hormones are peptide-like

A

(nor)epinephrine, melatonin, serotonin

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35
Q

T3/4 transport in blood

A

Bound to plasma proteins

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36
Q

Amine hormone receptors

A

T3/4 - intracellular
(nor)epinephrine, melatonin, serotonin - GPCR

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37
Q

Enzyme-linked receptor examples

A

Receptor tyrosine kinase receptor (RTK) - phosphorylation activates relay proteins. (insulin)
Cytokine type 1 receptor - JAK activates STAT (prolactin)

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38
Q

GPCR subunits

A

Gaq - phospholipase C > DAG > PKC
Gaq - phospholipase C > IP3 > Ca channel
Gas - AC > cAMP
Gai - inhibits AC > decrease cAMP. Increase phosphodiesterase (breaks down cAMP)

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39
Q

Melatonin production

A

Retina receives light > SCN > pineal gland > inhibit melatonin release

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40
Q

Eicosanoids

A

Hormone-like lipids derived from arachidonic acid. Involved in inflammation, immunity, ovulation, blood flow, uterine contractions

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41
Q

What is humoral stimuli

A

Non-hormone components in blood - Ca, glucose

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42
Q

Humoral stimulus endocrine reflex example

A

PTH: low Ca stimulates PTH release, stimulates Ca release from bone, kidney and GI Ca reabsorption

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43
Q

What hormones have only tropic effects and what does this mean?

A

FHS, LH, TSH, ACTH. Stimulate hormone production from another endocrine organ

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44
Q

What hormones have only non-tropic effects and what does this mean

A

Prolactin, MSH. Stimulate target organ directly

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45
Q

What hormone has both tropic and non-tropic effects

A

GH

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46
Q

What is ACTH and function. Stimulated by?

A

Adrenocorticotropic hormone - stimulates adrenal cortex to secrete cortisol and androgens. Stimulated by CRH

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47
Q

Production of oxytocin and vasopressin (ADH) in hypothalamus and transport to pituitary

A

Cell bodies of large neurons in hypothalamic nuclei - paraventricular nucleus (PVN) and supraoptic nucleus (SON) - produce the peptide neurohormones oxytocin and ADH. Transported in vesicles down axon (hypothalamic-hypophyseal tract) to post pituitary

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48
Q

Releasing and inhibiting hormone production in hypothalamus and transport to pituitary

A

Small neuron cell bodies in arcuate nucleus and paraventricular nucleus (PVN) produce releasing and inhibiting hormones. Released to median eminence, through hypothalamic-hypophyseal portal system to ant pituitary.

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49
Q

a) ADH function
b) Oxytocin function

A

a) Water retention
b) Bonding, lactation, uterine contractions

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50
Q

Anterior pituitary gland cell (hormone released)

A

Gonadotropes (gonadotropins - FSH, LH)
Somatotropes (somatotropin (GH))
Thyrotropes (TSH)
Corticotropes (ACTH)
Lactotropes (prolactin)

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51
Q

Another word for pituitary gland - ant, post

A

hypophysis - adenohypophysis, neurohypophysis

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52
Q

Embryological development of pituitary

A

Cells from roof of developing mouth (stomodeum - surface ectoderm) form ant. pituitary. Cells from base of brain (diencephalon - neuroectoderm) form post pituitary. Where lobes meet is Rathke’s pouch.

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53
Q

Primary vs secondary endocrine disorders

A

Primary affects target organ. Secondary affects hypothalamus or pituitary. In a pituitary disorder, damage of pituitary gland is primary disorder, damage of hypothalamic stalk is secondary disorder.

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54
Q

Hypopituitarism causes

A

Acquired - tumours (non-functioning micro/macroadenomas on pituitary, craniopharyngioma on stalk) and associated treatment
- Head injury
Congenital - genetic

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55
Q

Hyperpituitarism cause- effect

A

Caused by tumours:
Prolactinomas – excess prolactin secretion (most common)
GH-secreting adenomas – excess GH
TSHoma – excess TSH
Cushing’s disease – excess ACTH

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56
Q

GH/IGF-1 (somatotropin) axis.

A

a) Hypothalamus (GHIH/GHRH) > ant pituitary (GH) > liver and other somatic cells (IGF-1).

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57
Q

GH hyperfunction disorders (hyperpituitarism)

A

Gigantism from GH secreting tumour in pre-adolescent. Associated with hyperglycaemia. (bone elongation)
Acromegaly in post-adolescent. Associated with type 2 diabetes symptoms. (bone thickening). Diabetogenic effect - increased glucose stimulates insulin > insulin resistance and beta cell degeneration

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58
Q

IGF-1/GH deficiency (hypopituitarism) disorders

A

Dwarfism (pre adolescence):
African pygmies have inability to produce IGF-1
Laron dwarfism - GH receptor mutation - no IGF-1
(post adolescence): increase fat, insulin resistance, lethargy, adrenal insufficiency, infertility, diabetes associated, muscle weakness

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59
Q

Function of GH

A

GH stimulates bone elongation (before epiphyseal fusion) and bone thickening (after fusion). Increases muscle mass and protein synthesis. regulates BGL, stimulates lipolysis, decrease glucose uptake by muscle, increase glucose production (liver/kidneys)

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60
Q

Function of IGF-1

A

IGF-1 binds to insulin receptors and IGF receptors. Antagonist effect - increase lipolysis, FA uptake by muscle. Insulin-like effect - opposes GH: decrease gluconeogenesis (kidney), increase glucose uptake muscle

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61
Q

GH in fasting and fed states

A

Fasting (pre-prandial): GH increased, insulin low, glycogenolysis and gluconeogenesis, lipolysis
Fed (post-prandial): GH suppressed, insulin increases, increase glucose uptake in skeletal muscle, glycogenesis, adipogenesis/lipogenesis.

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62
Q

Tests to measure hormone levels

A

Static - of direct hormone or surrogate marker. e.g C peptide is marker of insulin. IGFBP of IGF.
Dynamic - suppression test (glucose test diagnoses acromegaly). Stimulation test (ACTH injection determines primary/secondary disorder)

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63
Q

Treatment for hypofunction disorders

A

Replacement of peripheral hormone, drugs that reduce resistance.

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64
Q

Treatment for hyperfunction disorders

A

Radiation therapy, surgery, suppression drugs, receptor antagonists

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65
Q

Where are parathyroid glands located

A

On posterior of thymus

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66
Q

Blood supply to thyroid/parathyroid. Venous drainage

A

superior and inferior thyroid arteries. superior, middle and inferior thyroid veins + thyroid plexus

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67
Q

Thyroid follicle composition and function

A

Follicular cells and colloid cavity - produce T3 and T4 (and thyroglobulin)

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68
Q

Parafollicular (C) cells produce

A

Calcitonin

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69
Q

What cell is found in parathyroid gland and what does it produce

A

Chief cells produce parathyroid hormone

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70
Q

What are oxyphil cells? function?

A

Derived from chief cells, lower PTH

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71
Q

What weeks of gestation does thyroid develop in

A

3-7

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72
Q

Initial proliferation of thyroid cells occur at the _ and then descends via _ to the trachea

A

foramen cecum, thyroglossal duct

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73
Q

Abnormalities with thyroid descent (3)

A

Persistent thyroglossal duct, pyramidal lobe of thyroid, ectopic thyroid tissue

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74
Q

What develops from the 3rd pharyngeal pouch

A

thymus and inferior parathyroid glands.

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75
Q

What develops from 4th pharyngeal pouch

A

dorsal - superior parathyroid glands, ventral - parafollicular cells

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76
Q

Abnormalities with parathyroid glands (2)

A

ectopic - inferior glands remain with thymus
supernumerary - glands may split causing an additional gland in neck

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77
Q

Thyroid hormone production

A

thyroglobulin (has tyrosine residues) produced by follicular cell is exocytosed to colloid. Iodide from blood is transported through follicular cell to colloid then oxidised to iodine by thyroid peroxidase (TPO). thyroglobulin + iodine (organification). thyroglobulin now has iodinated tyrosine residues. Conjugation, endocytosis into follicular cell, + lysosome > protein degradation > T3 (triiodothyronine) /T4 (thyroxine) transported into blood. All of T4 produced in thyroid. 80% T3 produced by peripheral conversion

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78
Q

How is T4 converted to T3 or rT3

A

Via tissue-based deiodinases.

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79
Q

Which thyroid hormone is more active (4x)

A

T3

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80
Q

What is reverse T3 *clue: hibernating bears

A

An inactive isoform of T3, binds to thyroid receptors - is an antagonist and competitive inhibitor for T4-T3 conversion. Thus reducing T3, causing hypothyroidism and slowing metabolism

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81
Q

Thyroid hormone receptor activation + function

A

They have intracellular receptors. Pass membrane by monocarboxylate transporters (MCT), bind at hormone response element to regulate gene expression of Na/K ATPase pump. Use of ATP stimulates mechanisms to increase ATP such as increasing basal metabolic rate - increase glucose uptake, glycolysis/KREBS > by-product is heat, insulin production to balance

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82
Q

Hypothalamus/pituitary/thyroid (HPT) axis

A

Stimuli: needs increase in metabolism e.g. exercise
H: thyrotropin-releasing hormone (TRH)
P: thyroid-stimulating hormone (TSH)
T: T4/T3

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83
Q

How does TSH stimulate thyroid hormone production (5)

A

Increases activity of iodide pump, increases secretion of thyroglobulin into colloid, increases TPO activity, increases lysosomal protein degradation to release T3 and T4, increases size and total number of thyroid cells

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84
Q

What is Grave’s disease

A

Excess stimulation of TSH receptors from antibodies

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85
Q

How is a goitre formed

A

Excess function of thyroid causes enlargement/hypertrophy

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86
Q

Thyroid hormone effect on liver

A

Increases gluconeogenesis, glycogenolysis, LDL receptors (to increase cholesterol/triglyceride uptake)
> increase glucose uptake, ATP use and decrease FA/cholesterol

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87
Q

Thyroid hormone effect on adipose

A

Increases hormone-sensitive lipase activity and lipolysis
> decrease fat stores and glucose available (from glycerol)

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88
Q

Thyroid hormone effect on muscles

A

Stimulate type II fibers to increase strength. Excess and low thyroid cause muscle atrophy

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89
Q

Thyroid hormone effect on heart

A

Increase receptors for catecholamines. Increases B1 adrenergic receptors increase sensitivity of contractile cells in AV node
> increases HR, CO, SV and contractility

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90
Q

Thyroid hormone effect on vasculature

A

Increase B1 adrenergic receptors and decrease ANGII receptors
> increases vasodilation

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91
Q

Thyroid hormone effect on nervous system

A

Increases number of dendrites, myelination, and number of synapses
> NS excitation
excess can cause tremor and loss of sleep
low thyroid - NS depression

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92
Q

Thyroid hormone effect on GI tract

A

Increase insulin from pancreas, glucose absorption, contractility of gut, exocrine secretions
> gut motility and absorption

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93
Q

What is cretinism

A

Caused by chronic lack of thyroid hormones in development results in short statue, mental disability and thick facial features

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94
Q

Thyroid hormone effect on bone

A

Increases bone growth in children along with GH

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95
Q

Symptoms of hyperthyroidism

A

Weight loss, heat intolerance, erythema (red face), tremor, anxiety, diarrhoea, exophthalmos (protruding eyes), goitre tachycardia, muscle atrophy

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96
Q

Symptoms of hypothyroidism

A

Weight gain, cold intolerance, slow movement, bradycardia, constipation, myxoedema, maybe goitre, short (pre-puberty), muscle atrophy, hypercholesterolaemia, atherosclerosis and CV disease

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97
Q

Degrees of disorder (primary, secondary..)

A

Primary: thyroid problem
Secondary: pituitary problem
Tertiary: hypothalamus
Quaternary: tissue insensitivity

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98
Q

What is thyrotoxicosis

A

The effect of excess thyroid

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99
Q

Grave’s disease

A

Autoimmune disease - antibodies stimulate TSH receptors on follicular cells > high thyroid hormone levels. TSH and THRH are low from negative feedback. Antibodies to thyroglobulin and to the thyroid hormones may also be produced. Swelling of eyes as the thyroid gland and the extraocular muscles share a common antigen that is recognised by the antibodies - binding causes swelling of eyes. Orange skin is from antibodies under the skin causing an inflammatory reaction and subsequent fibrous plaques.

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100
Q

Hashimoto’s disease

A

mild/no symptoms at first, swelling of thyroid and difficulty swallowing. Autoimmune disease - antibodies destroy thyroid gland

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100
Q

what cells release parathyroid hormone

A

Chief cells in parathyroid gland

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101
Q

Tests to determine if hypo- or hyper thyroidism

A

Blood, iodine uptake, stimulation test (only hypo)

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102
Q

PTH is released in response to

A

low blood Ca activation of CaSR (GPCR) and high phosphate levels

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103
Q

Calcitriol is also called

A

Active Vit D

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104
Q

What releases calcitonin

A

parafollicular (c) cells in thyroid

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105
Q

Function of PTH

A

Increase blood Ca, reduce PO4: Increases bone resorption (releases Ca and PO4), increase Ca reabsorption from distal tubule kidney, decrease PO4 reabsorption

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106
Q

Function of calcitonin

A

Decrease blood Ca: decrease bone resorption (deposition of Ca and PO4 into bone), decrease Ca absorption from GI, decrease Ca and PO4 reabsorption from kidney,

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107
Q

Function of calcitriol (Vit D)

A

Increase blood Ca: increase Ca and PO4 absorption from GI (by binding to Vit D receptors to increase membrane Ca transporters and intracellular Ca binding protein, calbindin) and reabsorption from kidney, increase osteoclast activity (bone breakdown - release Ca and PO4)

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108
Q

Ca absorption from GI

A

Passive (paracellular) and active (calcitriol + VDR > Ca transporters + calbindin)

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109
Q

Hypercalcaemia causes and symptoms

A

hyperparathyroidism, dehydration, vit D excess.
Thirsty, frequent urination, nausea, vomiting, constipation, bone pain, depressed NS, heart palpitations, fainting

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110
Q

Hypocalcaemia causes and symptoms

A

hypoparathyroidism, autoimmune disease, low Mg, vitamins, kidney dysfunction.
weak nails, bone fractures, numbness in hands, feet and face, cramps, excitable NS, depression, hallucinations, memory loss

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111
Q

Hyperphosphataemia causes and symptoms

A

hypoparathyroidism - chronic kidney disease, metabolic/respiratory acidosis.
Pulls Ca from bones to try and balance - hypocalcemia, numbness, bone pain, itchy rash

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112
Q

Blood supply to suprarenal arteries

A

Superior, middle and inferior suprarenal arteries

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113
Q

Adrenal glands are also called

A

suprarenal glands

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114
Q

Blood drainage of adrenal glands

A

Single adrenal vein: R into IVC, L into left renal vein

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115
Q

What are the three zones of the cortex from ext to int

A

Zona glomerulosa, zona fasciculata and zona reticularis

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116
Q

What steroid hormones are produced from the zona glomerulosa (example)

A

mineralocorticoids (aldosterone)

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117
Q

What steroid hormones are produced from the zona fasciculata (example)

A

glucocorticoids (cortisol)

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118
Q

what steroid hormones are produced in the zona reticularis (example)

A

androgens (androstenedione and DHEA)

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119
Q

What cells are in the adrenal medulla and what do they produce

A

Chromaffin cells - catecholamines (derived from tyrosine)

120
Q

Adrenal cortex is derived from intermediate ___

A

mesoderm

121
Q

Adrenal medulla is derived from ___ (neural __ cells)

A

Ectoderm, crest

122
Q

Function of aldosterone

A

Increase blood Na, decrease blood K and H:
In collecting duct of kidney tubule - increases Na+ (and water) reabsorption and increases K+/H+ secretion/excretion

123
Q

Aldosterone effect on transporters at kidney lumen

A

Aldosterone binds to receptor (MR) in cell > nucleus > increases transcription of:
(apical surface): Na channels (ENaC), K channels (ROMK), H+ ATPase pump
(basolateral surface): Na/K ATPase pump

124
Q

Loss of aldosterone results in (3)

A

Loss of Na - dehydration, low BP hyperkalaemia (K+) - heart problems acidosis (H+) - low blood pH, low cardiac output
> death

125
Q

Excess of aldosterone results in

A

Na retention - high BP
hypokalaemia - fatigue, muscle weakness, slow digestion, headache, heart failure
Metabolic alkalosis - high blood pH, confusion, nausea

126
Q

RAAS system: Angiotensinogen from the __ is converted into angiotensin I via __ from the __ converted to angiotensin II via __ from the __. Ang II stimulates __ and __ activity

A

liver, renin, kidneys, ACE, lungs. vasoconstriction and aldosterone synthase
> aldosterone

127
Q

how does atrial natriuretic peptide (ANP) effect aldosterone

A

It opposes it; aldosterone increase BP, detected by stretch receptors in atrium, ANP released. ANP inhibits aldosterone synthase, opposes ANGII, inhibits release of ADH from pituitary

128
Q

How is ACTH permissible for aldosterone production (but not regulatory)

A

ACTH produces cortisol, aldosterone can be derived from cortisol precursor.

129
Q

Function of cortisol (4)

A

Fight or flight; (1) glucose mobilisation (gluconeogenesis, lipolysis, decrease aa uptake) (2) maintain blood pressure (increased in chronic) (3) decrease inflammation (4) decrease non-essential processes (digestion..)

130
Q

Where is cortisol de-activated

A

At the tissues where MC receptors are abundant e.g kidney (we want mineralocorticoids not glucocorticoids acting here) - oxidation via 11-b-HSD2 to cortisone

131
Q

Where is cortisol re-activated

A

liver, lung, muscle, brain, adipose - where GC receptors are - reduction via 11-b-HSD1 from cortisone to cortisol

132
Q

How does chronic stress (cortisol) increase BP

A

cortisol acts on nuclear receptors to increase transcription of ADH and adrenergic receptors in vasculature (constriction), cortisol also acts on MC receptors in kidney to increase Na (and water) reabsorption

133
Q

Effects of chronic stress (4-5)

A

Increases BP, insulin resistance and insulinaemia (cortisol opposes insulin - increasing blood glucose), hyperglycaemia, tissue breakdown

134
Q

What is natriuresis

A

Excretion of Na

135
Q

What is diuresis

A

Loss of water

136
Q

How is cortisol anti-inflammatory and immunosuppresent (4)

A

Cortisol decreases expression of adhesion molecules to reduce inflammatory cell migration into tissue
Stabilises lysosome cell membrane to prevent release of inflammatory molecules from damaged cells.
Reduces cytokine IL-1 release (the cause of fever)
Suppress T lymphocytes

137
Q

Effects of cortisol that differ in acute vs chronic

A

Acute: appetite repressed, increase memory formation
Chronic: appetite stimulated, infertility via hypothalamic suppression, decrease memory retrieval

138
Q

How is cortisol regulated

A

Circadian rhythm and stress (psychological and physical)

139
Q

HPA axis for cortisol

A

H: CRH release from paraventricular nucleus (PVN)
P: ACTH from corticotropes
A: Cortisol via proliferation of cortical cells and production of steroidogenic enzymes

140
Q

Are androgens steroid hormones?

A

yes

141
Q

What do adrenal androgens do

A

Stimulate male characteristics

142
Q

Why do adrenal androgens have a greater role in females?

A

Because the male androgen testosterone is produced in the testes

143
Q

When are adrenal androgens produced

A

During adrenarche (maturation of adrenal cortex) which is pre-puberty (age 6-10) when zona reticularis develops. Peaks at age 20 and declines afterwards.

144
Q

What stimulates adrenal androgen production

A

ACTH

145
Q

Role of adrenal androgens in males

A

Normal early pubertal changes, if there is an excess leads to early (precocious) puberty. Little affect in males due to testes

146
Q

Role of adrenal androgens in females

A

Development of hair, acne and libido in puberty. Excess causes masculinisation and virilisation. In adult contributes to libido, muscle and bone mass, energy and strength. In post-menopause produces oestrogen (ovaries are now gone)

147
Q

Adrenal androgens are converted to __ in tissues

A

Testosterone and oestrogen

148
Q

Addison’s disease

A

primary adrenal insufficiency - reduction in all adrenal hormones

149
Q

Secondary and tertiary adrenal insufficiency effect on adrenal hormones

A

Decreased ACTH causes a decrease in cortisol and androgens with unchanged aldosterone (not controlled by HPA axis)

150
Q

Signs and symptoms of Addisons disease

A

Same as low aldosterone and cortisol. Loss of Na - dehydration, low BP; hyperkalaemia (K+) - heart problems; acidosis (H+) - low blood pH, low cardiac output; fatigue, weight loss, nausea, fainting, joint pain, hyperpigmentation.

151
Q

Why does Addisons disease have hyperpigmentation

A

ACTH is produced from pro-opiomelanocortin gene (PMOC gene). Gene produces both ACTH and MSH. Addisons is primary so high ACTH = high MSH

152
Q

What is Addisonian crisis

A

Occurs in people with low cortisol/aldosterone when a moment of stress occurs such as infection, dehydration, withdrawal of exogenous steroids. Cannot support blood pressure, glucose needs etc.. Causes fainting, hypoglycaemia (coma), confusion, cardiac arrest

153
Q

Conn’s syndrome

A

Primary hyperaldosteronism - excess aldosterone. Associated with low renin (-ve feedback via RAAS)

154
Q

Secondary hyper-aldosteronism

A

high aldosterone and high renin.
Causes: renin-secreting adenoma or renal hypoperfusion (reduction in blood flow)

155
Q

pseudo hyper-aldosteronism

A

increase in aldosterone effects + activation of MRs. Causes: inactivating mutation in 11B-HSD2 (cortisol inactivating enzyme), cross reactivity of other compounds (e.g liquorice on MR), Cushing’s syndrome (ectopic ACTH production), Liddles syndrome (ENaC activating mutation)

156
Q

Cushing’s syndrome

A

hypercorticolism - excess cortisol production. Primary (e.g adenoma) or secondary (pituitary - Cushing’s Disease or ectopic production)

157
Q

Cushings disease

A

Secondary hypercorticolism caused by pituitary problems. Excess ACTH

158
Q

Congenital Adrenal Hyperplasia

A

Hyperandrogenism - excess adrenal androgens. Mutation in steroidogenic enzymes (21 alpha hydroxylase) inhibits ACTH from producing cortisol or aldosterone and shunts pathway to produces androgens.

159
Q

Effect of hypercorticolism

A

Diabetogenic effect (excess glucose, insulin resistance), protein breakdown - muscle and bone wastage, Na retention + K loss (cortisol acts on MR at high levels), cardiac hypertrophy and obesity (chronic stress)

160
Q

Effects of hyperandrogenism

A

Aldosterone loss - salt loss, cortisol loss - adrenal failure, excess androgens - virilisation (in females), early puberty (in males)

161
Q

Adrenal pheochromocytoma

A

Tumour in adrenal medulla, excess catecholamines, 5Ps: pressure, palpitations, perspiration, pain, pallor

162
Q

Cells in pancreatic islets function; α, β, δ

A

α - glucagon, β - Insulin and amylin,
δ - somatostatin (inhibits glucagon and insulin to make nutrients available in blood for longer)

163
Q

Mechanism behind glucose stimulating insulin release

A

Glucose enters β cell via GLUT 2 transporter.
Undergoes oxidation to produce ATP closing of ATP/K channel - K is trapped inside > depolarisation.
Opening of Ca channels, Ca into beta cell, insulin exocytosed.

164
Q

Proinsulin >

A

insulin + C-peptide

165
Q

How does insulin decrease blood glucose

A

Insulin binds to membrane receptor > insulin receptor substrates (IRS) are
phosphorylated (P) > Downstream pathways create new proteins or change existing ones - moves GLUT onto membrane > Glucose uptake is increased (excl CNS). Insulin also inactivates enzyme that turns glycogen to glucose and opposes lipolysis

166
Q

Where are GLUT 2 and GLUT 4 found?

A

GLUT2 in liver and pancreas, GLUT4 in skeletal muscle and fat

167
Q

Amylin functions (4)

A

opposes glucagon, promotes satiety, not involved in glucose uptake, delays gastric emptying

168
Q

Neural control of BGL - Parasympathetic and sympathetic control of glycaemia

A

Para: stimulated by GI distension, β cells have ACh receptors that activated cause insulin release, decrease BGL
Symp: stress or exercise, noradrenaline increases glucagon activity, increase BGL

169
Q

Hormonal control of BGL (glycaemia)

A

GH, cortisol, adrenaline: in response to stress, increase BGL
Incretin (GLP1, GIP): released from GIT in
response to luminal nutrients, decrease BGL

170
Q

Type 1 diabetes vs Type 2 diabetes

A

Type 1: autoimmune destruction of β cells - hyperglycaemia, hypoinsulinaemia
Type 2: insulin resistance - hyperglycaemia, hyperinsulinaemia
adv type 2 β cells exhausted and die

171
Q

Why is blood test for glucose-bound Hb more accurate than RBC

A

Hb has a longer half life

172
Q

How does an oral glucose tolerance test/uptake test work

A

overnight fast, consume glucose, if glucose doesnt decrease after 2 hours = Diabetes

173
Q

Treatments for Type 1 diabetes (3)

A

exogenous insulin (bolus injection before food, basal injections for the day), insulin pump (automated infusion), fluid replacement (hyperglycaemia leads to glucosuria leads to polyuria)

174
Q

Treatments for type 2 diabetes (5)

A

sulfonylurea drugs increase insulin, metformin suppresses gluconeogenesis,
SGLT - sodium glucose transporter inhibitors - inhibit glucose reabsorption
fluid replacement for polyuria
Exercise decreases visceral fat insulin signalling

175
Q

Effect of too little insulin (increased glucose) (4)

A

Circulatory shock: hyperglycaemia and glucosuria - decreased water reabsorption > hypotension > sympathetic response)
Ketonaemia: Diabetic ketoacidosis (lipolysis > fatty acids converted to ketones > decreased blood pH (metabolic acidosis)
and compensatory hyperventilation (Kussmaul breathing))
Macrovascular complications: lipolysis > glycerol > arteriosclerosis + excess LDL > artherosclerosis&raquo_space; hypertension and ischaemia - foot ulcers and poor wound healing
Microvasular complications: certain tissues dont have cells that rely on insulin

176
Q

Effect of too much insulin (1)

A

Hypoglycaemia: Neuroglycopaenia (reduced ATP in neurons > reduced Na-K-ATPase activity > reduced APs > impaired cognition or consciousness)

177
Q

Hormonal risk factors for Type 2 diabetes

A

Cushings - excess cortisol and acromegaly - excess GH

178
Q

Kidney blood supply

A

renal arteries from aorta
renal veins > IVC

179
Q

the medulla and cortex of the suprarenal glands are derived from

A

medulla: neural crest – ectoderm
cortex: mesoderm

180
Q

blood supply to suprarenal glands

A

renal artery, aorta, inferior phrenic arteries

181
Q

what is vesicoureteral reflux

A

Detrusor muscle forms physiological sphincter, weakness of this muscle allows for back flow known as vesicoureteral reflux

182
Q

where is kidney referred pain to

A

lumbar back, inguinal region, lower abdomen, flank, groin

183
Q

Functions of kidneys (7)

A

1 Regulation of water and electrolytes
2 Excretion of waste (urea, creatinine, bilirubin, toxins)
3 Regulation of pH
4 Regulation of BP via renin
5 EPO production > erythropoiesis (RBC production). Stimulated by hypoxia.
6 Production of active vit D
7 Regulation of glucose metabolism. Make glucose from glutamine in cortex (ammonia by product)

184
Q

order of urine flow from kidney

A

minor calyx > major calyx > renal pelvis > ureter

185
Q

medulla consists of renal ___

A

pyramids

186
Q

renal corpuscle consists of

A

glomerulus (capillaries) and Bowman’s capsule. contains mesangial cells for support + can contract to change diameter of capillary > changes GFR

187
Q

what type of cells in PCT

A

cuboidal with microvilli

188
Q

Cortical vs medulla nephrons

A

location of renal corpuscle, cortical have short LOH

189
Q

what blood vessel is around the LOH

A

peritubular capillaries

190
Q

what ions mainly inside cell

A

K, PO4

191
Q

what ions mainly outside cell

A

Na, Cl, HCO3

192
Q

True or false: water n solute reabsorption can be regulated separately

A

true

193
Q

How is water reabsorbed in nephron

A

paracellular by osmosis or transcellular via aquaporins (channels) in both membranes of cell (apical and basolateral)
> both in PCT, mainly transcellular in distal nephron

194
Q

triple whammy for kidney injury

A

one diuretic, one ACEi/ARB, one NSAID

195
Q

why are ACEi not good for kidney failure

A

ACEi > no ANG II > no aldosterone actions > no K excretion > hyperkalaemia
renal impairment may affect drug excretion

196
Q

ACEi suffix

A

-pril

197
Q

ARB suffix

A

-sartan

198
Q

Adverse effects of ACEi

A

non-productive cough, hyperkalaemia, hypotension

199
Q

Clinical indications for ACEi (reasons to take)

A

hypertension, chronic heart failure

200
Q

adverse effects of ARB

A

hyperkalaemia, dizziness, headache

201
Q

clinical indications of ARB

A

heart failure, hypertension

202
Q

contraindication for ARB and ACEi

A

renal failure

203
Q

What is acute kidney injury

A

sudden decline in kidney function with decreased GFR and accumulation of waste products

204
Q

What are the three types of AKI

A

pre renal, intra renal and post renal

205
Q

Causes of pre renal AKI

A

Hypovolemia, shock, interruption of blood flow to kidneys

206
Q

Four subtypes of intra renal AKI

A

Glomerular disease, vascular disease, tubular disease, interstitial disease

207
Q

Chronic kidney disease defined as

A

GFR <60ml/min for 3 months or longer

208
Q

Common causes of chronic kidney disease

A

systemic diseases - hypertension, diabetes
kidney disease - AKI, stones
vascular disorders -

209
Q

Chronic kidney disease effects

A

Brain function (nitrogenous waste)
anorexia and vomiting (nitrogenous waste)
hypertension
anaemia (low EPO)
bone abnormalities (altered Ca)
oedema
change in circulating volume and electrolytes

210
Q

peritubular myoid cell function

A

contractile for sperm ejection

211
Q

Spermatogenesis

A

In seminiferous tubules:
Puberty: 1 spermatogonium undergoes mitosis to form 2 primary spermatocyte which undergoes meiosis 1 > 2 secondary spermatocyte > meiosis 2 > 4 spermatid > spermiogenesis in epididymis > 4 spermatozoa
requires T and ABP

212
Q

Sertoli cell function

A

form blood testis barrier
stimulate meiosis via testicular fluid
secrete ABP
secrete inhibin B
secrete anti-mullerian hormone to stop female characteristics developing

213
Q

Leydig cell function

A

Produce 95% T and DHT

214
Q

What is amplification pathway

A

Conversion of T to DHT via enzyme 5-alpha reductase

215
Q

DHT function

A
  • External genitalia (scrotum, penis, testes), - Testes descent (with T)
  • Prostate enlargement
  • Secondary male characteristics: facial hair, baldness, acne
216
Q

What is aromatisation/diversification pathway

A

Conversion of T to estradiol/estrogen via aromatase enzyme in testis and peripherally

217
Q

what type of hormone/receptor are T and DHT

A

steroid hormones with androgen receptors

218
Q

estradiol function in males

A

testes - spermatazoa motility
prostate - water reabsorption
bone - closure of epiphyseal plate
brain - good mood

219
Q

What causes prenatal androgen surge

A

hCG from maternal placenta stimulates Leydig cells to produce T

220
Q

Testosterone functions

A
  • Wolffian duct stimulation > internal genitalia (SEED - seminal vesicle, ejaculatory duct, epididymis, ductus/vas deferens
  • Spermatogenesis
  • Testes descent (with DHT)
  • Secondary sex characteristics
  • Increase BMR
221
Q

what causes puberty/pubertal surge of T in males

A

KNDy neurons in hypothalamus > KISS1 > GnRH neurons > GnRH
pulsatile release of KISS 1 and GnRH

222
Q

Stimuli that suppress KISS1 release

A

Energy imbalance, excess prolactin,
hyper/hypo thyroid hormones, cortisol

223
Q

what is imprinting in male development

A

Expression of XY genes
SRY gene > TDF protein

224
Q

How does tumour in pineal gland lead to hypergonadism

A

Pineal gland > melatonin > prolactin > inhibits KISS1
Reduced melatonin = more KISS1 = more GnRH = more T/DHT

225
Q

Features of hypergonadism in males

A

early/exacerbated puberty - lower voice, high libido, hair loss, reduced fertility from
-ve feedback

226
Q

Features of hypogonadism in males

A

loss of secondary sex characteristics
infertility

227
Q

Where does gametogenesis occur in males/females

A

males - semineferous tubules
females - ovaries

228
Q

Oogenesis

A

Foetus: Primordial germ cell > oogonium > mitosis > million primary oocytes held in prophase of meiosis I > birth
Puberty, each month: completion of meiosis I > secondary oocyte held in metaphase of meiosis II + first polar body
Fertilisation: complete meiosis II > ovum/ova > gamete + second polar body

229
Q

What is ovulated each month

A

secondary oocyte in metaphse II

230
Q

Where does secondary oocyte form

A

in ovarian follicles

231
Q

Ovarian cycle:

A

Follicular phase: primary oocyte in follicle (theca and granulosa cells) >
FSH - granulosa cells - estrogen , LH - theca cells - androgen precursors > follicle grows from primordial to Graafian follicle, antrum forms, secondary oocyte forms in the Graafian follicle
Peak of estradiol to stimulate proliferation
Ovulatory phase: theca cells contract and release enzymes to break through capsule, granulosa cells release prostaglandins > Graafian follicle ruptures releasing one secondary oocyte (ovulation)
Peak in LH/FSH, inhibin B reduces FSH after peak
Luteal phase: follicle become corpus luteum (luteal cells) produce progesterone (and oestrogen) to prepare endometrium, and inhibin A to reduce FSH/LH
LH stimulates progesterone from luteal cells
Pregnancy maintains corpus luteum by placenta hormone hCG - keep high progesterone. Placenta also produces inhibin A. After wk 12 placenta takes over from corpus luteum to produce progesterone.
No pregnancy: Corpus luteum > corpus albicans

232
Q

Theca cells produce
granulosa cells produce

A

Theca: androgens - T,
Granulosa: convert T to estradiol, inhibin to reduce FSH

233
Q

When does pre-antral phase end and antral phase begins

A

When from many secondary follicles, one tertiary follicle (Graafian follicle) arises

234
Q

What is the corona radiata

A

Layer of granulosa cells that surround zona pellucida (which surrounds secondary oocyte) for protection and nutrients

235
Q

What covers secondary oocyte when it is ovulated

A

glycoprotein layer - zona pellucida and corona radiata (granulosa cells) for protection

236
Q

What movements move the secondary oocyte from infundibulum to uterus

A

Ciliary action and peristalsis

237
Q

Uterine/menstrual cycle

A

Menstrual phase: ABSENCE of P and E > functional layer: spiral arteries constrict
> ischaemia of functionale, cell death, enzymes, endometrium breakdown
Basal layer: remains to provide cells for next cycle.
Myometrium at its thinnest and contracts.
Proliferative phase: ESTROGENS from follicle > zona functionalis grows: mitosis of basal stromal cells + glandular epithelial.
Followed by cell hyperplasia + increased extracellular matrix to thicken layer.
Myometrium thickens, uterine gland proliferates
Secretory phase: After ovulation, PROGESTERONE and oestrogen from corpus luteum > secretions from endometrium, vascularisation, glycogen storage in decidual cells, endometrium thickening. P prevents contractions of myometrium, stops sloughing (bleeding). Oestrogen > growth of uterus and mammary glands, uterus contractions in birth

238
Q

Overlap of uterine and ovarian cycles

A

Proliferative phase of uterine over follicular phase of ovarian (estradiol from follicle stimulates zona functionalis growth).
Secretory = luteal

239
Q

what class are estrogen and progestrone receptors

A

nuclear and GPCR

240
Q

Source of oestrogen production

A

mainly ovaries but also bone, adipose, liver, skin, brain > aromatisation

241
Q

FSH affect on granulosa cells

A

Increase proliferation
Increase aromatase enzyme (to convert androgen precursor to estrogen)

242
Q

LH affect on theca cells

A

proliferation, enzyme for androgen precursor, produce some progesterone

243
Q

Estradiol affect on granulosa cells

A

+ve feedback. Increase LH and FSH receptors and sensitivty > peak of FSH/LH before ovulation
Larger LH due to -ve feedback from inhibin from granulosa cells

244
Q

Sex hormones in breast development

A

oestrogen - fat deposition, induces ductal formation
progestrone - develops lobules and alveoli
Prolactin > milk production (+stops menstruation)
Oxytocin > milk ejection

245
Q

primary vs secondary amenorrhea

A

Primary - never menstruated
Secondary - previously present but been
>6 months
Oligomenorrhea - irregular periods

246
Q

Menopause cause

A

Exhaustion of follicles - lose a bunch each cycle (only one goes through whole cycle)
No more E and P
remaining hormones from adrenal glands and aromatisation

247
Q

What is functional hypothalamic amenorrhea

A

Secondary type of amenorrhea caused by energy deficit:
weight loss, stress, high exercise (Athlete), low leptin > suppress GnRH

248
Q

POCS

A

Secondary type of amenorrhea - excess androgens from ovaries from altered GnRH pulse > higher LH than FSH
Accompanied by excess insulin

249
Q

What is hormonal imprinting

A

First encounter between receptor and ligand - develops normal connection for life. Critical period is pre-natal

250
Q

Misimprinting

A

high or low ligand concentration, related molecule binds. Dependant on time of misprint.

251
Q

Faulty imprinting

A

Endocrine disrupters (found in food, contaminants) can displace endogenous hormones or have antagonist/agonist effects (stimulate or inhibit hormonal pathways)

252
Q

EDC effects

A

Bones and growth, reproductives, metabolism, cancer

253
Q

What is foetal programming model / The Barker Hypothesis

A

Prenatal exposures have lifelong consequences
e.g low birth weight > increased risk of chronic adult diseases due to brain sparing (other organ development is second). Followed by post-natal excess nutrition > type II diabetes
Underdeveloped:
- kidneys lead to hypertension (decreased nephron number).
- Pancreas (decreased B cells) and liver/fat/muscle (decreased IGF-1) lead to type 2 diabetes.
- altered HPA axis > increased cortisol > hypertension + obesity

254
Q

Cortisol HPA axis in mum and baby

A

placental CRH stimulates mum and baby axis. Maternal and foetal cortisol stimulate placental CRH (+ve)
11- beta HSD enzyme in placenta breaks down cortisol into cortisone so excess maternal cortisol doesn’t affect baby. Chronic elevated maternal cortisol can overwhelm 11-beta HSD and elevate foetal cortisol > affecting foetal HPA axis

255
Q

cortisol in pregnancy

A

Important for foetal maturation, parturition (birth)
Elevated maternal cortisol leads to shortened gestation (quicker parturition)

256
Q

What is early life stress

A

Social and psychological stressors affect later life health e.g abuse as a child may lead to drug abuse as an adult due to neural plasticity as brain still developing post natal.
Childhood abuse can lead to methylation of glucocorticoid receptor > affects cortisol
ELS > decreased oxytocin

257
Q

Significance of organisational-activational hypothesis

A

It is not circulating adult hormones that determine sex characteristics - it is those around birth (prenatal and slightly after)

258
Q

What is the organisational-activational hypothesis

A

Organisation: Prenatal/neonatal exposure to gonadal steroids (sex hormones) is important for permanent sexual differentiation of brain and behaviour
Activation: secondary surge of sex hormones at puberty for sex-dependant behaviours (mostly in males)

259
Q

True or False: both sex and gender can affect epigenetics that affect all systems of body

A

True

260
Q

List some factors that can influence phenotype

A

Fetal programming
Organisation-activation hypothesis
ELS
Hormonal imprinting:mis- and faulty
Sex/gender

261
Q

Are aboriginals less likely to have type I diabetes

A

Yes

262
Q

A reason for aboriginal health problems

A

Barker hypothesis, low socioeconomics affect maternal health > high stress > affects foetal HPA axis > diabetes type II

263
Q

Urogenital develops from

A

intermediate mesoderm

264
Q

Urine production starts week

A

9

265
Q

Waste from foetal urine goes to

A

maternal blood to be cleared by her kidneys

266
Q

what is cryptorchidism

A

one or both testes fail to descend into scrotum. Could become cancerous

267
Q

what is testicular ectopia

A

in strange place - abdomen, femoral region

268
Q

If sperm is not ejactulated it is

A

reabsorbed by macrophages in epididymis

269
Q

what is hypospadias

A

urethra opens prematurely

270
Q

what produces seminal fluid

A

60% by seminal vesicles, 35% prostate, bulbourethral glands
> all still produce seminal fluid after vasectomy
(vas deferens that transport sperm are cut)

271
Q

testicular hydrocele

A

fluid accumulation in two layers of tunica vaginalis

272
Q

what nerve supplies the cremaster muscle

A

genitofemoral

273
Q

is penis in superficial or deep perineal pouch

A

superficial

274
Q

pelvic diaphragm muscles

A

levator ani (puborectalis, pubococcygeus, iliococcygeus) + coccygeus

275
Q

ovarian artery is a branch of

A

abdominal aorta

276
Q

suspensory ligament contains blood and nerves for

A

ovaries

277
Q

where does fertilisation typically occur

A

in the ampulla

278
Q

ligaments that support uterus

A

pubocervical, transverse cervical and uterosacral

279
Q

Uterine wall layers (3)

A

Perimetrium: serosa - outer layer
Myometrium: smooth muscle, blood vessels and lymphatics - stratum vasculature. This layer hypertrophy in pregnancy.
Endometrium: 2 layers:
stratum basale
stratum functionale - shed in mestruation

280
Q

Blood supply in uterine wall

A

uterine artery > arcuate artery > radial branch > spiral artery + straight artery
Straight supplies stratum basale

281
Q

Testicular and ovarian cancer inflames

A

para-aortic lymph nodes

282
Q

Glomerular filtration barrier

A

Glomerular capillary fenestrated endothelium, -ve basal lamina (3 layers), foot processes of podocytes

283
Q

Pressures that determine filtration rate

A

Hydrostatic pressure (60): pressure from blood in glomerular capillaries causing filtration (high BP = higher hydrostatic pressure = more filtration)
Colloid/oncotic osmotic pressure (32): pressure from proteins in blood opposes filtration (high protein in glomerular capillary = less filtration)
Bowman’s capsule hydrostatic pressure (18): pressure from filtrate in capsule - opposes filtration (kidney stones block outflow = build up of filtrate in capsule = less filtration)
4th force in unhealthy individuals is colloid osmotic pressure in Bowman’s capsule from proteins that pass through

284
Q

What is osmolarity

A

Concentration of solutes - high solutes = high osmolarity

285
Q

Factors that affect GFR

A

Either affect pressures: renal blood flow, blood pressure affected
or filtration coefficient (Kf): filtration barrier or slit surface area affected.

286
Q

what is autoregulation in kidneys

A

Maintains GFR over range of high blood pressures. Consists of myogenic response and tubuloglomerular feedback.

287
Q

What is the myogenic response

A

Myogenic: high BP > stretch > smooth muscle Na channels open > stored Ca released > Ca binds to actin > contraction > afferent arteriole constriction

288
Q

What is tubuloglomerular feedback

A

Macula densa in DCT detects tubular NaCl: High GFR = high NaCl in tubule = macula densa signal afferent arteriole to constrict (via ATP release) > reduce GFR

Low GFR = low NaCl = macula densa produce prostaglandins + NO > vasodilation of afferent arteriole.
Also signal juxtaglomerular/granular cells to secrete renin > RAAS, aldosterone increases Na channels in nephron, ang II causes efferent vasoconstriction

289
Q

Nephritic Syndrome

A

Acute inflammation - severe. Post-infectious, damage to glomerular basement membrane so severe RBCs can pass > (1) haematuria. (2) Oedema from protein loss, (3) hypertension from RAAS activation lowers GFR = (4) oliguria (less urine).

290
Q

Nephrotic Syndrome

A

chronic inflammation. injury to podocytes, immune-complex deposition, scarring/thickening of entire capillary wall. (1) High proteinuria, liver cannot compensate - (2) low albumin. Fluid from tissues is normally attracted into capillaries from protein - drop in oncotic pressure from loss of proteins > (3) oedema. (4) hyperlipidemia

291
Q

What would neutrophils in nephron indicate

A

Acute inflammation - damage to podocytes and endothelial cells by immune cells - affects glomerular filtration rate

292
Q

Goodpasture’s

A

autoimmune disease - affects basement membrane of kidneys and lungs - life threatening. type II - antibody mediated

293
Q

systemic lupus

A

circulating immune complexes - type III, deposit at sites of high filtration b/n basement membrane and endothelial cells causing inflammation

294
Q

diabetic mellitus

A

reduced glucose reabsorption:
increased urine osmolarity
reduced water reabsorption
increased urine - diuresis and polyuria
increased plasma osmolarity - high glucose in blood > excess thirst (polydipsia)

295
Q

diabetes insipidus

A

lack of vasopressin (ADH) production or response:
decreased water reabsorption > high Na
increased urine - polyuria
dehydrated - polydipsia - increased thirst
fatigue
constipation
nocturnal enuresis - bed wetting
Treatment: desmopressin nasal spray + hydration

296
Q

syndrome of inappropriate ADH secretion (SIADH)

A

Oversecretion of ADH when normal BP, low [electrolyte]
water reabsorption
dilutes Na - hyponatraemia - confusion, weakness, headache, personality change, coma
Treatment: fluid restriction, hypertonic saline, V2R blockers

297
Q
A

Year 2 Session 2 (4 decks)

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