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Year 5 Path Chemical Pathology > Year 1: Endocrinology > Flashcards

Year 1: Endocrinology Flashcards

1
Q

endocrine gland

A

group of cells which secrete messenger molecules directly into blood

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2
Q

neurotransmitters

A

chemical signal which transmits informtation over a chemical synapse (from neuron to other target cell)

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3
Q

List the three classification groups of hormones

A

Polypeptide/ Protein Hormones

Steroid Hormones

Miscellaneous Hormones (don´t fit into either category)

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4
Q

Synthesis of Protein Hormones

A

Via Gene expression:

  • pro hormone mRNA
  • translation of rough ER
  • transfered to Golgi for Processing

–> Packed into vesicles with enzyme to cleave pro-hormone (activation)

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5
Q

Synthesis of Steroid Hormones

A
  • all derive from cholesterol (stored in vesicles in cell)
  • released by Esterase
  • transport into Mitochondria (StAR - protein) (often rate-limiting step)

processing by enzymes in mitochondria

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6
Q

Storage of Protein Hormones

A

Stored in Vesicles in Cells until secretion

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7
Q

Storage of Steroid Hormones

A
  • Stored in Blood

–> Bind to Plasma protein (e.g. Albumin (binds all steroid hormones) or specific plasma protein + some free hormones:

forms equilibrium: free hormones + free plasma protein = plasma bound protein

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8
Q

Receptors /direct effect of protein Hormones

A

G-protein coupled receptors

  • bind to receptors and all modify cell signaling
    (e. g. cAMP production, drives cholesterol production)
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9
Q

Receptos / direct effect of steroid hormones on cell

A

diffuse into cell (no membrane-boudn receptors required)

–> bind to intracellular target (receptor)

–> travel into nucleus with complex and regulate transcription

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10
Q

Positive feedback

A

A increases which causes B to increase which causes A to increase ( exponential growth, rather unstable)

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11
Q

Negative feedback

A

Negative feedback: secretion and production of hormone is controlled by released product (high concentration of product = low production /secretion of hormone)

–> controll of hormones (gives stability)

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12
Q

Location of hypophysis

A

beneath hypothalamus

in sella turcica

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13
Q

Hypothalmic nucleus

A

collection of neural cell bodies in hypothalamus

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14
Q

List Five (Six) Hormones produced by Adenohypophysis

A

Somatotrophin

Prolactin

Thyroid stimmulating Hormone (TSH, THyrotrophin)

Luteinsing Hormone (LH), Follicle Stimmulating Hormone (FSH)

Adenocorticotrophic Hormone (ACTH, Corticotrophin)

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15
Q

Somatrophin (cells, Hopothalamic Hormones, Effect)

A

Cells: Somotrophs

Hypothalamic Hormones: up: Growth Hormone / Somatrophin releasing Hormone (GHRH); down: Somatostatin

Effect:

growth: direct (on cells) indirect (on liver –> IGF 1)

– increased metabolism (protein synthesis, gluconeogenesis, fatty acid production, cartilage + somatic cell growth)

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16
Q

Prolactin (cells, Hypothalamic Hormones, Effect)

A

Cells: Lactotrophs

Hypothalamic Hormones: down (constant) Dopamine

up: Thyrotropin-releasing hormone (TRH)

Effect:

Mild production (suppression of Dopamine)

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17
Q

Control of Somatotrophin

A

Stimmuli on Hypothalamus: Sleep, oestrogen, stress, fasting, Gherline (from stomach))

Negative feedback:

IGF on Hypothalamus and Adenohyoophysis

Somatotrophin (GH) on Hypothalamus

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18
Q

Control of Prolactine

A

Stimmulus: Suckling on Breast + TRH

Suppression of Dopamineproduction by Hypothalamus

–> Milk secretion

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19
Q

Thyroid Stimmulating Hormone (cells, hypothalamic hormones, effect)

A

Cells: Thyrotrophs

Hormones: up: TRH (Thyrotrpin Releasing Hormone)

Effect:

On Thyroid

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20
Q

LH and FSH (cells, hypothalamic hormones, effect)

A

Cells: Gonadotrophs

Hormones: Gonadotrophin releasing hormone (GnRH)

Effect:

Ovaries and Testicles

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21
Q

Adenocorticotrphic hormone (ACTH) (cells, hypothalamic hormones, effect)

A

Cells: Corticotrophs

Hormones: UP: Cocticotrophin releasing hormone, Vasopressin

Effect:

Adrenal cortex

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22
Q

Median eminence

A

Area which connects adenohypohysis with neurones,

Many blood vessels

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23
Q

Magnocellular neurones

A

terminate in neurohypohysis

(cell bodies both in paraventricular and supraoptic nuclei found)

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24
Q

Parvocellular neurones

A

terminate in either median eminence or other part of brain

(cell bodies only found in paraventricular nuclei)

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25
Q

Supraoptic neurons

A

Go from Supraoptic nuclei to Neurohypophysis (Magnocellular neurons)

Store Hormones in Herring bodies

Either produce Vasopressin or Oxytocin

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26
Q

Paraventricular neurons

A

derive from paraventricular neucleus to neurohypohysis (Magnocellular neurones, majority) or other parts + median eminence (parvocellular neurones)

Produce either vasopressin or oxytocin

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27
Q

Structural difference vasopressin, oxytocin

A

2AA differ

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28
Q

Synthesis of Vasopressin and Oxytocin

A

Pre-Prohormone (with Signaling peptide)

–> Prohormone (cleavage for activation:

Vasopressin+Neurophysin+Glycopeptide

Oxytocin + Neurophysin (slightly different)

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29
Q

Compare differnet receptors for vasopressin

A
  • V1: in atherial smooth muscle + adenohypophysis (ACTH production)
  • linked to G-protein + phospholypase C (up: Ca2+, IP3, DAG in cell) –> Vasoconstriction
  1. V2: water reabsorbtion in duct cells (antidiuretic effect)
  2. linked to G-Protein and cAMP production –> induces travel of Aquapoins (AQP2) to lumen of kidney
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30
Q

Feddback control for Vasopressin

A

Stimmuli: Plasma osmolarity up (reabsorbtio of water required)

BP down ( vasoconstriction required, a bit less relevant)

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31
Q

Polydipsia

A

inceased thirst

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32
Q

Polyuria

A

increased volume of urine

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33
Q

Disregulatin of Vasopressin

A

Diabetis insipidus:

No reuptake /little reabsorbtion of water

–> polydipsia + polyuria

Central/cranial = no VP produced

Nephrogenic = resistance to VP

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34
Q

Summarise the effects of Oxytocin on several organ systems

A

On Uterus

  • contraction of myometrial cells in uterus –> delivery of baby (+ encanced productio of prostoglandins which make cervix softer + dilate)

On Mammary glands:

  • Contracti on of myoepithelial cells –> Milk ejection (no milk production)

CNS: Tend and Befriend

Other effects: temporary vasodilaition, vasoconstriction of umbilicus, on kideny: Vasopressin -like effects

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35
Q

Regulatio of Oxytocin

A
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36
Q

Dysregulation of Oxytocin

A

No / too little milk ejection

induction of labout might be required

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37
Q

Which factors (Hormones) regulate Blood glucose level? (Feedback Loop)

A

It is controlled via blood glucose levels:

Down: Insulin

Up: Glucagon, Cortisol, Somatotrophin, Catecholamines

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38
Q

How gets glucose into cells?(and effect of insulin on it)

A

Via GLUT-4, Insulin enhanced Glucose transporter (7times higher with Insulin)

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39
Q

Islets of Langerhans

A

2% of pancreatic tissue

a,ß, delta cells

paracrine regulation

gap junctions allow small molecules to pass, tight junctions allow small intercellular spaces to form

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40
Q

a- pancreatic cells

A

secrete Glucagon

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41
Q

pancreatic ß cells

A

secrete insulin

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42
Q

pancreatic delta cells

A

secrete somatostatin

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43
Q

Synthesis of Insulin

A

Synthesis of pre-pro insulin

–> cleaved: proInsulin + C-peptide (secreted 1:1 into blood)

posttranslational modification:

Insulin (two chains, connected through disulfide bonds)

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44
Q

When is insulin secreted?

What effects does insulin have?

A
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45
Q

When is Glucagon Secreted?

What are the effects?

A

+ Proteolysis

+ ketone body production

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46
Q

What is the Incretine effect? How is is achived?

A

More insulin is secreted after a meal compared to IV glucose

–> Glucagon-Like-Peptide (GLP1)

–> promotes insulin, supresses glucagon

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47
Q

DM type 1: patophysiology and clinical features

A

Diabetes Type 1:

Insulin deficiency because of autoimmune reaction to ß-cells

  • proteolysis and weight loss
  • Hyperglycaemia
  • Polydipsia, Polyuria
  • Ketouria
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48
Q

DM type 2: patophysiology and clinical features

A

Insuline resistance:

–> no problem with receptors! –> insulin as growth hormone still works, but no metabolic activity

60-80% OBESE.

* Dyslipidaemia (abnormal fat content in blood)

* Later insulin deficiency (exhaustion of beta cells).

* Hyperglycaemia.

* Fewer osmotic symptoms.

* T2DM presents with complications whereas T1DM hardly ever presents with complications.

–> resides in liver, muscle and adipose tissue

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49
Q

Explain relationship between dyslipidemia, hypertension and insulin resistance

A

dyslipidemia: hypertension in LDL which is associated with Ischaemic heart disease and atherosclerosis –> hypertension

No insulin= no uptake of triglycerides into cell but only release –> free fatty acids (mainly LDL)

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50
Q

Metabolic effects of insulin resistance

A

increase in NEFA (non-essential fatty acids), tryglycerides, LDL cholesterol

  • decrease in: HDL, lipoprotein lipase activity, VLDL clearance

–> enough insulin present to suppress proteolysis and ketone production –> no ketones in urine and no weight loss

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51
Q

Explaint the Anatomy of thyroid gland and a thyroid follicle

A
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52
Q

Basal metabolic rate

A

Grundumsatz

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53
Q

Explain the Synthesis of thyroid hormones

A
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54
Q

Explain Mechanism of action of thyroid hormones

A

T4 gets into T3

–> stimulation of Protein synthesis via binding toTHR (Thyroid hormone receptor) in nucleus

+ less important: T3 non-nuclear actions on ion-channels

+ metabolic stimulation of cell

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55
Q

Actions/Effect of Thyroid hormones

A

fetal growth and development

  • increases basal metabolic rate –> carbohydrate, fat and protein metabolism
  • potential increase of catecholamines –> adrenaline, dopamine etc. –> increases heart rate, lipolysis etc.
  • also effects on GI, CNS and reproductive symptoms
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56
Q

Control of TH production

A
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57
Q

Wolff-Chaikoff- Effect

A

Iodine inhibits release of Thyroid horomones (for about 17 days)

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58
Q

Where does the thyroid gland originates from?

A

back of tounge (thyro glossal dot) (average ca. 20g)

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59
Q

What is the foramen caecum of the tounge?

A

Little dot at apex of tounge due to thyroid development (disappearing thyroid duct)

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60
Q

Anatomy of the thyroid

A

Weight: 20g

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61
Q

Three possible problems with thyroid

A

Agenisis (no formation)

Incomplete descent (e.g. Lingual thyroid)

Thyroglossal cyst

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62
Q

Effects of Agenesis of thyroid (or total lack of thyroxin)

A

Cretin:

  • irreversible brain damage bc of lack of thyroxin

Treatment/ prevention: Life-long replacement

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63
Q

Simple thyroxin sinthesis diagram

A
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64
Q

Compare thyroglobulin and thyroxin binding globulin

A

Thyroglobulin: protein in colloid of follicular cell , storage of thyroxin

Thyroxin binding globulin TBG: protein in blood that binds to Thyroxine in blood ( 75% bind, 1% free)

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65
Q

Pimary hypothyroism (cause, effects, symptoms)

A

-Primary thyroid failure (myxoedema)

damage = autoimmune

Up: TSH, down: T3+T4

Symptoms

  • fatigue,
  • cold intolerance
  • depression
  • weight gain
  • less appetite
  • bradycardia
  • costipation (verstopfung) –> a lot because of decrease of basal metabolic rate + no help in catecholamides

–> eventually

myxoedemal coma

66
Q

Hyperthyroidism symptoms + reason

A

Autoimmune –> antibodies stimmulate TSH receptors on thyroid

  • inceased basal metablic rate:
  • raised temperature,
  • increased appetide,
  • weight loss,
  • tachycardia,
  • myopathy,
  • mood swings,
  • tiredness,
  • diarrhea,
  • tremor of hands
67
Q

Graves Disease

A

Autoimmune disease

Symptomps of hyperthyroidism

+ Sore + swollen eyes –> 2nd antibodies on eye

non-pitiing ptetibial myxoedema –> growth of soft tissue in ankle region (3rd. antibodies)

68
Q

Anatomy of Adrenals

A

Medulla =produces catecholamines (e.g.adrenaline)

Cortex –> produces cortecosteroids (e.g. aldosterone, cortisol* sex steroids)

69
Q

Which Zones in Adrenals produce which hormones?

Binding of the two hormones in blood

Glucocorticoid + mineralcorticoid

A

+ Medulla = catecholamides

Glucocorticoid: colesterole (only 10 % free)

Mineralcorticoid: Aldosterone (45% free)

70
Q

To which receptors do Aldosterone and Cortisol bind?

A

Aldosterone: Bind to Mineralcorticoid receptors

Cortisol Bind to Glucocorticoid receptors + Mineralcorticoid receptors

–> some tissues are prodected from cortisol by 11bhsd2 so aldosterone has a task to do (Kidney + Placenta)

71
Q

When is aldosterone secreted?

A

Angiotensinogin —Renin—> Angiotensin 1

(Renin : low BP, low Na2+, sympathetic renal activity)

Angiotensin 1 —ACE—> Angiotensin 2

Angiotensin 2 –> stimulates Aldosterone secretion (can be also stimulated by low Na+ and high K+ but to a lesser extent)

72
Q

Effects of Aldosterone + Mechanism of action

A

Effect on Kidney (collecting duct)

-> reabsorbtion of Na2+ (Transcrtiption of proteins: sodium chanel formation + Na2+/K+ ATPase active pump of Na2+ into blood –> loss of potassium)

73
Q

Feedback control of cortisol

A
74
Q

Mechanism of Action of Cortisol + effects

A

highly binds to MR, Partly binds to GR

Metabolic actions: central glucose availability and storage

up: gluconeogenesis, glycogenesis
down: peripheral glucose storages, uptake of fatty acids in skeletal muscleand fat tissue, reduction of blood flow in these tissues)

Memory: pro memory (up: serotonin receptors) (down for supraphysological effects)

Immune: Anti-inflammatory and immunosupressive

75
Q

Addisons disease (cause, clinical features, management)

A

Primary adrenal failure –> lack of cortisol

Causes

  1. autoimmune desease damages adrenal cortex
  2. TB of adrenal gonads

Features

  • Tanning (A lot of ACTH released –> hypothalamus wants to make more Cortisol –> POMC is cleaved into ACTH and MSH (Melanocyte stimulating hormone)
  • Salt loss (low sodium, high potassium levels)
  • Hypotonic
  • weight loss, decreased appetite
  • fatigue

Management

  • IV saline for rehydration and sodium intake
  • IV glucose
  • oral steroid hormone replacements
76
Q

Cushing`s syndrome (causes + features)

A

High cholesterol levels

Causes

  • Oral replacement /intake of steroid hormones
  • Pituitary adenoma(Cushing`s disease)
  • Adrenal adenoma/carcinoma
  • Ectopic ACTH (lung cancer)

Clinical features

  • diabetes (long times of high blood glucose levels)
  • weight gain (redistribution: central weight, thin legs and arms, excessive nuchal fat, moon face)
  • Skin (acne, facial hair, thin, easy bruise, striae (stretch marks))
  • proximal myopathy –> reduction of protein and muscle + osteoporosis
  • depression
  • hypertension
  • immunosupression (poor wound healing, reactivation of TB)
77
Q

Conn’s syndrome

A

Cause:Aldosterone Adenoma

Features:

Hypertension

Oedema

high Na+, Low K+

78
Q

Primary + secondary amenorrhoea

A

Primary amenorrhoea:

never had period

Secondary amenorrhoea:

have had normal periods, but don’t have it anymore

79
Q

Oogenesis

A

gametogenesis in females

oogonia “freezed” untill puberty

80
Q

Spermatogenesis

A

begins at puberty

81
Q

Hypothalamo-Pituitary-Testicle Axis

A

FSH: gametogenesis

LH: hormone production

82
Q

Describe the main Main structures in testis from spermatogenesis to urethra

A

1. Coiles seminiferous tubules (spermatogenesis)

  • -> formes tubules –> Seitoli cells (Spermatogenesis; FSH sensitive)
    2. Rete testis and Vasa efferentia –> connect coiles siminiferous and vas dererens
    3. Epididymis (storage of sperms)
    4. Vas deferens (to urethra)

Next to it: Leydig cells –> produce and secrete hormones, LH sensitive

83
Q

Andrgoens physical actions (fetus + adults)

A

Main active component: Dihydroxitestosterone (reduction)

Fetus: development of genital organs in men, growth of fetus

Adults: spermatogenesis, anabolism of bone + muscle, development of prim, 2nd. sex characteristics, growth in puberty, sexual behavioral (conversion into oestrogen in brain)

84
Q

Oestrogens definition + physical actions

A

Definition:Everything that induces proliferation of endometrium Mainly: 17ß-oestradiol

  • triggers LH—> ovulation, breast growth, skin, vaginal secretion, behavioral, osteoblast stimmulation, metabolic actions
85
Q

Definiton and physical actions Progestrogens

A

Anything that changes secretory activity of endometrium

Mainly: Progesterone

stimmulates secretion of endometrium and cervix

increases basal body temperature, growth of alveolar in breasts etc.

86
Q

What are the Main Structure in Ovaries?

A
87
Q

Hypothalao-ovarian axis

A

Changes within menstrual cycle (feedback) + production

88
Q

Definiton and reason for infertitliy

A

Definiton: no pregnancy after 12 month of unprotected sex

pituitary failure, prolactinoma (prolactin inhibits LH/FSH), Testicular failure, ovarian failure, polycystic ovarian syndrome

89
Q

Main phases and hormone levels in menstrual cycle (better overview in notes)

A
  1. Early follicular phase (follicles in ovaries develop FSH) follicles slowly produce E2
  2. Early-mid-follicular phase (one follicle gets bigger than others, production of oestrogen, + feedback loop oestrogen, granulosa cells)
  3. Mid-follicular phase (low FSH kills smaller follicles, development of Graafian follicle produces E2)
  4. Late-follicular phase: extremelx high E2, +feedback on LH FSH, high levels of E2 stimmulate ovulation
  5. Luteral phase (corupus luteum (rest of follicle) produces high amounts of progesterone) preperation for implantation

–> no fertilization:stron neg. feedback –> low levels –> menstruation

90
Q

Physiological functions of calcium

A
  • Neuromuscular excitability
  • Muscle contraction
  • Strength in bones
  • Intracellular second messenger
  • Intracellular co-enzyme
  • Hormone/neurotransmitter stimulus-secretion coupling
  • Blood coagulation (factor IV)
91
Q

What are the action of PTH

A

Parathyroid horomne (synthesized there)

–> up calcium

92
Q

PTH regulation Feedback

A
93
Q

DIHYDROXY-CHOLECALCIFEROL actions

A

gegenspieler gegen knochenabbau und PO43- ausscheidung

–> preserves bone

94
Q

Action and regulation of Calcitonin

A

Synthesized in parafollicular cells of thyroid

95
Q

Phosphate control

A

More reabsorbtion:

1,25 (OH)2 D3 in kidney and small intestine

Release by PTH when breaking down bones –> thats why excreted by PTH

Excretion:

Directly PTH + Calcitonin

Fibroblst Growth Factor 23 (FGF 23) –> Kidney excretion (high levels of phosphate and VitD3) –> protection from too much phosphate

96
Q

Sings and causes for hypocalcaemia

A

Signs :easy exitable cells : Hand and cheek contraction

  1. Hypoparathyroidism (ideopathic, low magnesium)
  2. Pseudo-hypoparathyroidism (resistance to PTH)
  3. Vit D deficiency (sign: bone matrix too thin (bowing, fractures)
97
Q

Hypercalcaemia (reasons, differentiation between primary, secondary and tertiary hyperparathyroidism)

A

Resons:

  1. Primary hyperparathyroidism –> adenoma (no negative feedback)
    (2. Secondary hyperparathyroidism (no hypercalcaemia)–>chronic low Ca2+–> kidney disease (no reabsorbtion possbile, no synthesis of 1,25 (OH)2 D3))
  2. Tertiary Hyperparathyroidism —> reason for secondary is cured –> but parathyroids went autonomous, dont respod to feedback anymore
  3. Too much Vitamin D3
98
Q

What is the effect of Somatotrophin on the body?

A
99
Q

How does the V1a receptor of Vasopressin woirk? (intracellular mechanism)

A

phospholipase C

  1. PIP2 into inositol triphosphate IP3(and diacyl glycerol, DAG)
  2. which increase cytoplasmic [Ca2+] and other intracellular mediators (PKC)
  3. which produce a cellular response
100
Q

How does the V2 receptor of vasopressin work? (cellular mechanism)

A

linked via G proteins to adenylcyclase

which acts on ATP to form cyclic AMP

which activates protein kinase A

which in turn activates other intracellular mediators

which produce cellular response (aquaporins, AQP2)

101
Q

What may be the clinical use of oxytocin?

A

Induction of Labour at term

  • controlled i.v.infusion

Prevention+ treatment of post-partum hemorrhage

  • Slow i.v.injection/infusion
  • Local pressor action in uterus suppresses bleeding

•FACILITATION OF MILK LET-DOWN

  • Intranasal spray

•AUTISM – SOCIAL RESPONSIVENESS??

  • Intranasal spray
102
Q

What is Acromegaly?

What are its symptoms?

A

It is an excess of growth hormones –> overproduction of Somatrophin

  • organs enlarge
  • body continues to grow
103
Q

What is a normal glucose level? (mMol)

A

4-5mmol

104
Q

What are the effects of insulin secretion

A

Decreases Blood glucose

  • Increased glycogenesis
  • Increased glycolysis
  • increased uptake of glucose via GLUT-4 transporters

Increased Protein synthesis and Amino-acid transport

Increased lipogenesis, decreased lipolysis

105
Q

When is insulin secreted?

A

Mainly: low blood golucose

But also

  • certain AA
  • Glucagon
  • GI hormones
  • PNS
106
Q

Which effect does somatostatin have on insulin and glucagon secretion?

A

It inhibits both, insulin and glucagon secretion

107
Q

What are the effects of Glucagon secretion?

A

Increased blood glucose

Increased heptic glcogenolysis

Increased gluconeogenesis

  • AA transport into liver
  • Lypolysis
108
Q

Which effect does Glucokinase have on insulin secretion?

How?

A

Glucokinase (Hexokinase IV) transforms Glucose into Glucose-6-phosphate –>

sets off intercellular pathways that trigger insulin release

  1. ATP generation
  2. Blockage of ATP-sensitive K+ channel
  3. allows Ca2+ influx
  4. Triggers insulin secretion
109
Q

Which molecule is also referred to the Insulin Glucose sensing molecule?

A

Glucokinase

110
Q

Through which receptor does glucose enter a pancreatic ß-cell?

A

Through the GLUT-2

111
Q

Compare insulin storage in healthy individuals and individuals with DMT2

A

In healthy individuals: Stored insulin is present

In DMT2 –> they don’t have stored insulin resulting in steeper increase in blood glucose

112
Q

What is thyroxine?

A

T4 (thyroid hormone)

113
Q

How are thyroid hormones transported in the blood?

A
  1. 70-80% thyroid-binding globulin
  2. albumin (10-15%)
  3. prealbumin

•Only 0.05% T4 and 0.5% T3 unbound (bioactive components)

114
Q

What is the main hormone product of the thyroid?

A

T4 is mainly produced (though T3 is the bioactive form)

115
Q

Which nerve runs close to the thymus? What does it supply?

A

the left recurrent laryngeal nerve is close (supplie the vocal cords)

116
Q

what is the function of the colloid of the thyroid?

A

It stores thyroglobulin and Thyroxine (also iodinisation + formation of T3/T4 happens here)

117
Q

What is myxoedema?

A

It is primary hypothyroidism

118
Q

How would blood levels for Thyroxine and TSH be in primary hypothyroidism?

A

It would be a low Thyroxine (can’t be produced) and high TSH (doesn’t receive negative feedback)

119
Q

How are the effects of untreated hypothyroidism and how is it treated

A

Patients will die untreated–> high cholesterol leading to stokes and heart attacks

Treatment: Just replacement of T3/4 (monitor until TSH is normal)

120
Q

Which factor in the adrenals determines, which hormone is produced (e.g. aldosterone and not cortisol)

A

It is the different content/concentration of the enzymes in different zones (e.g. aldosterone/cortisol only 2 enzymes differ)

low level for reproductive hormone enzymes

121
Q

How is aldosterone transported in the blood?

A
  • 40% free
  • 15% bound to CBG =corticosteroid binding globulin
  • 45% Albumin

–> A lot is free

122
Q

How is Cortisol transported in Blood?

A

Only 10% free

80% bound to CBG (Corticosteriod binding globulin)

10% Albumin

123
Q

Why do we have aldosterone, if cortisol can bind to both (MR and GR) receptors?

A

Some tissues are “protected” from cortisol (e.g. placenta, kidney)

11b-hydroxysteroid dehydrogenase 2 breaks down Cortisol into Cortisone (inactive)

124
Q

Why get people with primary adrenal failure get tanned?

A

Becaue of an increased production of ACTH

–> ACTH is a cleaving product of POMC, other product is MSH

MSH (melanocyte stimmulating hormone)

125
Q

Explain symptoms of primary adrenal failure (Addison’s disease)

A

no cortisol or aldosterone, so low blood pressure

  • Cortisol deficiency
  • Salt loss –> no Aldosterone
  • Low blood pressure –> No aldosterone
  • Eventual death
126
Q

How do you treat Addison’s disease?

A

Urgent treatment

  • Rehydrate with normal saline
  • •Give dextrose to prevent hypoglycaemiawhich could be due to the glucocorticoid deficiency
  • •give hydrocortisone or another glucocorticoid

–> Replacement of hormones

127
Q

What is the difference between Cushing’s syndrome and Cushing’s disease?

A

Syndrome= can be any cause of too much cortisol

Disease= Pituitary dependant (e.g. pituitary adenoma)

128
Q

Name four reasons for Cushing’s syndrome

A
  • Taking steroids by mouth (common)
  • pituitary-dependent Cushing’s disease (pituitary adenoma)
  • Ectopic ACTH (lung cancer)
  • adrenal adenoma or carcinoma
129
Q

How would a patient with Cushing’s syndrome present?

A

Hypercortisolism

Lemon on stick appearance

  • central weight gain
  • stretch marks
  • proximal myopathy
  • moon face
  • Diabetes –> long exposure to high glucose
  • thin skin, extra hair growth
  • hypertension

immunosuppression –> e.g. reactivation of TB?

130
Q

What are the side effects of (non-medical) use of steroids?

A
  • Hypertension
  • Diabetes
  • Osteoporosis
  • reactivation of infection (immunosuppression)
  • easy bruising
  • poor wound healing, thin skin
131
Q

How is the disease with an aldosterone-producing adenoma is called? What are its effects?

A

It is the Conn’s disease

  • hypertension
  • oedema
  • high Na+, low K+
132
Q

Explain the structure of a semeniferous tubule

A

Overall structure:

  1. Lumen with Spermatozoa
  2. Cell layer of Sertoli cells (Spermatogenesis, FSH sensitive)
  3. Zone with Spermatogonia
  4. Leydig cells associated with it (produce and secrete hormones, LH sensitive)
133
Q

What is the function of the Seretorli cells?

Which stimmulus do they respond to?

A

Are located at the cell layer in a seminiferous tubule

  • Spermatogenesis
  • FSH sensitive
  • Produce Inhibin in response to FSH
134
Q

Explain the location, control and function of the Leydig cells (in male)

A

Are outside Seminiferous tubule

produce androgens in response to LH (mainly testosterone)

135
Q

Explain the structure of a Graafian Follicle

A

From Outside to inside

  • Thecal cells (LH sensitive)
  • Granulosa cells (FSH)
  • Follicular Fluid
  • Ovum
136
Q

In which phase of the ovarian cycle is oestrogen produced?

Which effect does this have on the endometrium?

A

It is produced in the follicular phase of the ovarian cycle and promotes proliferation of the endometrium

137
Q

In which phase of the ovarian cycle is oestrogen and progesterone produced?

Which effect does it have on the endometrium?

A

It is produced in the Luteal phase and causes the secretory phase of the endometrium (preparation for arrival of the Egg)

138
Q

Explain the Levels of FSH and LH in the menstrual cycle and how they change

A

Both: about baseline til Follicular phase

139
Q

What is the first part of the menstrual cycle?

What happens during this phase?

A
  1. Early follicular face

FSH dependant development of the follicles in the ovaries

Follicles produce Progesterone and Oestradiol which has a negative feedback on Hypothalamus/Pituitary —> Levels fall

140
Q

What happens in the early-mid-follicular phase of the menstrual cycle?

Ho do levels of LH, FSH, Oestrodiol and Progesterone change?

A

The follicle most sensitive to FSH gets bigger –> induced autocrine feedback loop of E2

  • (more granulosa cells, produce more E2 (oestrogen), more oestrogen produce more granulosa cells

FSH and LH stay the same or fall slightly (because of feedback)

Progesterone does not change

Oestrogen increases

141
Q

What is the Graafian Follicle?

What happens to the other follicles?

What does it produce?

A

The largest follicle no longer requires FSH to develop and proliferate

A fall of FSH kills other follicles that can’t develop FSH independently

It keeps growing and producing large amounts of E2

142
Q

What happens during the mid-follicular phase?

A

Graafian follicle develops (produces E2)

other follicles get killed by fall of FSH

–> increase of oestradiol + inhibin

-ve feedback on FSH reduces levels,

No change in levels of LH/Progesterone

143
Q

What happens during late follicular phase of ovulation?

A

Extremly high levels of E2 (produced by Graafian Follicle) induce +ve feedback on GnRH and LH

High E2 levels of E2 and LH/GnRH trigger ovulation

144
Q

What happens during the Luteal phase of the menstrual cycle?

A

2nd phase of cycle

high levels of progesterone produced by Corpus Luteum

–> prepares for implantation

If no fertilisation: -ve feedback of inhibin, E2 and Progesterone on GnRH/ LH+FSH

145
Q

What is the bioactive form of Testosterone?

How is testosterone transported in blood and seminiferous fluid

A

Active form: DHT

–> Dihydrotestosterone

Transport:

  • 60% bound to Sex hormone binding globulin (SHBG, blood) or Androgen binding globulin (seminiferous fluid)
  • Albumin 38%
  • 2% free ( = bioactive)
146
Q

How is the bioactive form of Oestrogen?

A

E2= 17ß- Estradiol

147
Q

What kind of receptors does the Parathyroid hormone bind to?

What is its mechansim of action in the cell?

A

It binds to a G-protein coupled receptor–>

•Activation of adenyl cyclase, but also probably PLC as second messenger systems

148
Q

What do osteoblasts/osteoclast do?

What is their function in calcium metabolism?

A

Osteoblast:

  • Built bone (need Ca2+)
  • inhibited with Parathyroid hormone

Osteoclasts

  • break down bone (release Ca2+)
  • inhibited by Calcitonin/ stimulated by Parathyroid hormone
149
Q

What is the activated form of Vitamin D3? What are its Names?

A

1,25(OH)2 Vit D3, Calcitriol, dihydroxi-cholecalciferol

150
Q

WHat is the effect of Fibroblast-Growth factor 23?

A

It is a factor that influences Phosphate

  • is stimmulated by a combination of hight levels of Phospate and VitD3
  • Drives Phosphate secretion
  • Negative feedback on Calcitriol
151
Q

Which effect does insulin have on the GLUT-4 receptors?

Where are these receptors most abundant?

A

Insulin recruits the GLUT-4 receptor vesicles to the membrane when binding to the insulin receptors

They are most abundant in muscle and adipose tissue

152
Q

Through which receptor is Glucose taken up into muscle and adipose tissue?

A

Via the GLUT-4 receptor

153
Q

Which effects does Insulin have on proteins and muscle cells?

A
  • Insulin INHIBITS proteolysis, Cortisol STIMULATES it.
  • Insulin INHIBITS oxidation of amino-acids in the cell.
  • Insulin STIMULATES re-synthesis of proteins from amino-acids.
  • –> This means less amino-acids leave the cell to go to the liver to be used to produce glucose.
154
Q

Which hormones stimulate gluconeogenesis?

A

Glucagon

Somatotrophin

Cortisol

Catecholamines

155
Q

What is Hepatic glucose output? Which two processes normally contribute to this?

A

it is the amount of synthesized glucose that leaves the liver

There are two mechanisms:

  1. Gluconeogenesis
  2. Glycolysis
156
Q

Which effect does insulin have on the liver?

A

It stimmulates

  • protein synthesis
  • glycogen formation

It inhibits

  • Gluconeogenesis
  • Ketone-body production
  • Glycolysis
157
Q

Which effect does insulin have on adipose tissue?

A

It stimulates

  • Fat entering the cell (via activation of lipoprotein lipase)
  • Formation of triglycerides

It inhibits:

  • Lipolysis
158
Q

Which effect does cortisol have on the uptake of glucose into the cell?

A

It tends to inhibit uptake

159
Q

In which tissues is insulin resistance found?

What is the part that does not work properly?

A

Insulin resistance resides in the

  • LIVER
  • MUSCLE
  • ADIPOSE TISSUE

but note that the receptors for insulin are normally functioning, the post-receptor effect is faulty.

160
Q

Which substances are normally increased or decreased as a result of Type 2 diabetes?

A

Insulin resistance causes

An increase in

  • Non-esterified fatty acids
  • Triglyceride
  • LDL cholesterol

A decrease in

  • HDL
  • VLDL clearance (decrease in lipoprotein lipase)

Year 5 Path Chemical Pathology (24 decks)

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