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Disease, Diagnostics and Therapeutics > Hyperaldosteronism > Flashcards

Hyperaldosteronism Flashcards

1
Q 
test results show:
↓ Renin
↑ Aldosteronism
↔ Cortisol
What type of hyperaldosteronism is this
A

Secondary

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2
Q

What are the three ovarian cycle phases

A
  • follicular- pre-ovulation
  • follicular- late
  • luteal
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3
Q

What causes secondary hyperaldosteronism

A

occurs as a result of anything causing decreased blood flow/pressure to kidneys or lowered blood Na conc

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4
Q

what are the 3 types of dehydration

A

hypotonic/hyponatremic - primarily loss of electrolytes
hypertonic/hypernatremic - primarily loss of water
isotonic/isonatremic - equal loss of water and electrolytes

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5
Q

What is osmolarity effected by

A

is affected by changes in water content, as well as temperature and pressure

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6
Q

What is dipstick testing

A

A urine test strip or dipstick test is a basic diagnostic tool used to determine pathological changes in a patient’s urine in standard urinalysis

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7
Q

What is the role of LH

A

binds to the ovaries causing the production of oestrogen, conversion of the Graafian follicle into the corpus luteum (produces progesterone

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8
Q

what is ANP

A

released from the atria
due to stretch/distension
binds to natriuetic peptide receptor resulting in guanylate cyclase activity - increase cAMP
smooth muscle relaxation, vasodilation of affertent

causes a decrease in renin and subsequently angiotensin and aldostrone

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9
Q

How do you control blood pressure short term

A

Neural- the mechanoreceptors in the carotid and aortic bodies detect changes which travel via either the parasympathetic/sympathetic NS

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10
Q

What happens in primary hyperaldosteronism

A

high aldosterone level increases reabsorption of sodium/water and loss of potassium by the kidneys

results high blood pressure/hypertension
muscle weakness can occur if potassium levels are very low

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11
Q

Is t3 or t4 more active

A

T4 is less active than T3 but is secreted in greater amounts from the thyroid

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12
Q

What is renal autoregulation

A
  • the kidney itself can adjust the dilation or constriction of the afferent arterioles, which counteracts changes in blood pressure
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13
Q

what would indicate primary hyperaldosteronism in a sample

A

an increase in both renin and aldosterone

No change in cortisol

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14
Q

What is the osmolar gap

A

the difference between the measured osmolality and the calculated osmolarity

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15
Q

Give an example of a hormones produced in the Posterior PG

A

ADH /Vasopressin

Oxytocin

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16
Q

If a disease occurs at the pituitary axis, what type of disorder is it

A

Secondary

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17
Q

If cortisol doesn’t cause pseudohypoaldosteronism, what happens to it normally

A

11b-HSD2 converts it to cortisone

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18
Q

How do peptide hormones i.e. ADH or oxytocin cause vasoconstiction steps

A

Gaq –> PLC activated –> IP3 increased + DAG –> PKC –> phosphorylation of V1R = vasoconstriction

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19
Q

what is aldosterone

A

a hormone that regulates sodium and water retention by the kidney and the removal of potassium

important role in controlling blood pressure

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20
Q

What is a urine dipstick

A

A standard urine test strip may comprise up to 10 different chemical pads or reagents which react (change colour) when immersed in, and then removed from, a urine sample.

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21
Q

What are the effects t3 has on metabolism

A 
o	Increase glucose absorption
o	Increased glycogenolysis
o	Increased gluconeogenesis
o	Increased lipolysis
o	Increased protein catabolism
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22
Q

Give an example of a hormones produced in the hypothalamus

A

Thyrotropin RH
Corticotropin RH
Gonadotropin RH

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23
Q

What occurs in the PCT

A

reabsorption of o Glucose
o Amino Acids
o Other solutes such as phosphates and lactate
via sodium co transporters

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24
Q

What is a normal reference range of plasma osmolality

A

275-299 milli-osmoles / kg

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25
Q

what does angiotensin II stimulate

A

release of aldosterone
release of ADH
release of ANP
vasoconstriction

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26
Q

How does Hashimotos’ disease effect T3, T4 and TSH

A

Decreased T3 and T4, Increased TSH

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27
Q

what is plasma conc

A

conc of urine in blood after a IV injection

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28
Q

What two things are needed to breakdown cholesterol

A

ACTH and cholesterol desmolase

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29
Q

What are the main functions of the kidney

A

a regulator, excretor and producer

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30
Q

If fertilisation does not occur, what happens to the ovarian cycle

A
  • Corpus luteum degenerates spontaneously
  • Progesterone falls
  • Uterus loses its endocrine support
  • Menstruation
  • FSH & LH get to work again on the follicles
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31
Q

What is the key function of the loop of henle

A

to maintain the osmotic gradient for water reabsorption

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32
Q

Give an example of a hormones produced in the adrenal cortex

A

aldosterone

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33
Q

what is the effect of ADH

A 
released from the posterior pituitray 
increases fluid retention 
aquaporins in collecting duct 
V2R (Gs) stimulates aquaporins
stimulates Na2+ K+ 2Cl- cotransporter
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34
Q

where is aldosterone produced

A

in the adrenal glands - located at the top of each kidney

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35
Q

What does T3 cause

A

DNA transcription
mRNA translation
Protein Synthesis

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36
Q

What will increased osmolality of the blood stimulate

A

secretion of ADH, resulting in: increases water reabsorption, more concentrated urine, and less concentrated blood plasma.

37
Q

What may be tested using a urine disptick

A

Haematuria
Proteinuria
Glucose
UTI

38
Q

how is the GFR regulated

A

intrinsic mechanisms
- renal autoregualtion - vasocontrsiction/dilation

extrinsic mechaisms

  • neural/endocrine control - ANP = increase GFR
  • tubulogolmular feedback - specialised cells within the distal tubule monitor Na2+
39
Q

How does Graves’ disease effect T3, T4 and TSH

A

Increase T3 and T4, and decrease TSH

40
Q

Explain the steps of the RAAS

A
  1. BP decreases, so kidneys release renin into the blood
  2. Renin converts angiotensinogen into angiotensin 1
  3. Angiotensin 1 is converted to angiotensin II by ACE
  4. Angiotensin II causes vasoconstriction, and the release of aldosterone by the adrenal glands
  5. Aldosterone causes sodium retention and potassium excretion
41
Q

Give an example of a hormones produced in the thyroid

A

T3

T4

42
Q

If fertilisation does occur, what happens to the ovarian cycle

A
  • Corpus luteum maintained by hCG from the chorion
  • Becomes the Corpus Luteum of Pregnancy
  • Maintains uterine lining until placenta takes over as main producer of progesterone at 3 months
43
Q

What is the initial hormone stimulating the menstrual cycle

A

Gonadotrophin Releasing Hormone (GnRH)

44
Q

what is the glomerular filtration rate

A

rate of fluid filtered through the kidneys

estimates how much blood passes through the glomeruli each minute

45
Q

Where does water move in, and solutes move out, in the nephron

A

Thin ascending limb

46
Q

what is urine flow

A

amount of urine produced in a given time

47
Q

What is the hypothalamus

A

The portion of the brain which maintains homeostasis and links the endocrine and nervous systems

48
Q

Which cells in the kidney sense Na and CL in the tubular fluid

A

Macula densa cells

49
Q

Describe the steps in pseudo-hyperaldosteronism

A

cholesterol –> progesterone –> cortisol –> increased sodium reabsorption and K and H excretion

50
Q

What is osmolality affected by

A

is independent of temperature and pressure.

51
Q

What is pseudo-hyperaldosteronism

A

Cortisol is not converted into cortisone by 11B-HSD2 and so binds to mineralocorticoid receptors in the renal cells, causing the same effects as aldosterone

52
Q

What is the function of the thick ascending limb

A

actively reabsorbs sodium, potassium, and chloride. This is also impermeable to water

53
Q

define hypoaldosteronism

A

lack of aldosterone
occurs as part of adrenal insufficiency
causes dehydration, low bp, low Na and high potassium blood concs.

54
Q

What is the role of FSH

A

binds to the ovaries, stimulating the development of ovarian follicles, the secretion of oestrogen and the secretion of inhibin.

55
Q

How do you calculate mean arterial pressure

A

Q X Total peripheral resistance

56
Q

What are the two types of nephron

A

cortical and juxtamedullary

57
Q

what would indicate secondary hyperaldosteronism in a sample

A

High levels of serum and urine aldosterone, along with a low plasma renin
No change in cortisol

58
Q

What system controls long term BP

A

Renin-Angiotensin-Aldosterone System

59
Q 
test results show:
↓ Renin
↓ or ↔ Aldosteronism
↔ Cortisol
What type of hyperaldosteronism is this
A

Pseudo

60
Q

What is the role of progesterone

A

progesterone then causes the endometrium to become receptive to the implantation of the fertilised ovum.

61
Q

Give an example of a hormones produced in the Adrenal Medulla

A

Adrenaline/Noradrenaline

62
Q

Symptoms of Graves’ disease

A 
	Weight loss
	Goitre
	Ophthalmopathy
	Increased HR
	Sweating
	Tremor/anxiety
63
Q

What is Graves’ disease

A

1* Hyperthyrodism- Autoimmune antibodies signal to make thyroid hormones

64
Q

Where does water move out, and solutes move in, in the nephron

A

Thin descending limb

65
Q

How can arterioles/veins help short term control of blood pressure regulation

A

cause vaso/venoconstriction to increase BP

66
Q

What is Hashimoto’s disease

A

1* Hypothyroidism- Thyroid is destroyed, autoimmune thyroiditis

67
Q 
test results show:
↑ Renin
↑ Aldosteronism
↔ Cortisol
What type of hyperaldosteronism is this
A

Primary

68
Q

What are the effects t3 has on growth

A

o Bone maturation

o CNS maturation

69
Q

If a disease occurs at the glands, what type of disorder is it

A

primary

70
Q

Give an example of a hormones produced in the kidney

A

Renin

71
Q

How is absorbed water returned to the circulatory system in the kidney

A

Via the vasa recta

72
Q

What are the three major sections of the kidney

A

Cortex
Medulla
Renal Pelvis

73
Q

What are the effects t3 has on the cardiovascular system

A

o Increase in Q
o Increased B-adrenoreceptors
o Increased Ca2+ ATPases
o Increased myosin

74
Q

Give an example of a hormones produced in the Anterior PG

A 
Thyroid Stimulating H
Follicle Stimulating H
Luteinising H
Adrenal Cortico-Tropic H
Growth H
75
Q

How do steroid/thyroid hormones cause physiological actions

A

nuclear/cytoplasmic receptors bind DNA steroid receptor elements –> gene transcription –> mRNA –> new proteins

76
Q

What element is needed for T3 and T4 production

A

Iodine

77
Q

GFR equation

A

urine conc x urine flow/plasma conc

78
Q

what is the effect of aldosterone

A

increase Na2+ and fluid retention (distal convoluted and collecting duct)
loss K+ and H+ in the urine

79
Q

What are the 5 sections of a nephron

A
  • Glomerulus
  • PCT
  • Loop of Henle
  • DCT
  • Collecting Duct
80
Q

What are the effects t3 has on BMR

A

o Increased Na-K ATPase pump
o Increased oxygen consumption
o Heat production
o Increased BMR

81
Q

What is the counter-current multiplier effect

A

uses energy to create an osmotic gradient enabling the reabsorption of water, and production of concentrated urine. It moves sodium chloride from the tubular fluid into the interstitial space deep within the kidneys

82
Q

What receptors do angiotensin II use to cause vasoconstriction

A

AT1R

83
Q

What receptors do both cortisol and aldosterone bind to

A

mineralocorticoid receptors

84
Q

what causes primary hyperaldosteronism

A

caused by the overproduction of aldosterone in the adrenal glands
(usually by a benign tumour of one of the glands)

85
Q

What are normal GFR rates for males and females

A

males - 125ml/min

females - 105ml/min

86
Q

How is the kidney protected

A

encapsulated by a renal capsule, and further surrounded by adipose tissue

87
Q

Symptoms of Hashimoto’s disease

A 
weight gain.
fatigue.
paleness or puffiness of the face.
joint and muscle pain.
constipation.
inability to get warm.
88
Q

What is Neural (nervous system) control (GFR)

A

these extrinsic mechanisms can override renal autoregulation and decrease the glomerular filtration rate when necessary

89
Q

where is renin produced

A

In the kidney (juxtaglomerular apparatus)

Disease, Diagnostics and Therapeutics (14 decks)

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