Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 2 - Endocrinology (DP) > Physiology > Flashcards

Physiology Flashcards

1
Q

Where is the thyroid gland located?

A

Anterolateral to larynx and trachea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where are the parathyroid glands located?

A

Posterior aspect of each thyroid lobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What do thyroid follicles surround and what does it contain?

A

The colloid:

- Tyrosine-containing thyroglobulin filled sphere

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the process by which T3 and T4 are made and stored?

A
  1. Iodine taken up by follicle cells
  2. Iodine attaches to tyrosine residues on thyroglobulin:
    -Forms two units
    > Monoiodotyrosin unit (MIT)
    > Diiodotyrosine unit (DIT)
  3. Coupling of MIT and DIT:
    • MIT + DIT -> T3
    • DIT + DIT -> T4
  4. Stored in colloid thyroglobulin until required
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What thyroid hormone is secreted in larger amounts?

A

T4 (90% of secreted hormone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which thyroid hormone is more potent?

A

T3 (~4 times more potent than T4)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where is T4 converted to T3?

A

Liver

Kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What thyroid hormone is the major biologically active hormone?

A

T3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why do T3 and T4 bind to plasma proteins?

A

They are lipophilic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What plasma proteins do thyroid hormones bind to?

A

Thyroxine-Binding Globulin -> ~70%
Thyroxin-Binding Prealbumin -> ~20%
Albumin -> ~5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the other name for thyroxine-binding prealbumin?

A

Transthyretin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the features of T3 binding? What does this allow?

A

Bound 10-20 times less avidly by TBG
Not bound significantly by TTR
This allows more rapid onset and offset of action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does the metabolic state correlate closer to; level of free hormone of level of total plasma concentration?

A

Level of free hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does Ninewells asses thyroid hormones?

A

Measure fT3 and fT4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What can cause increased levels of thyroxine-binding globulin?

A 
Pregnancy
Newborn
Oral contraceptive (Increased oestrogen)
Tamoxifen
Hep A
Chronic Hepatitis
Billiary cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What can cause decreased levels of thyroxine-binding globulin?

A 
Androgens
Cushing's
Acromegaly
Severe systemic illness
Chronic liver disease
Nephrotic syndrome
Drugs:
     - Phenytoin
     - Carbamazepine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do carbimazole and propylthiouracil work?

A

Inhibit thyroperoxidase:

- Enzyme needed to produce MIT and DIT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does increased TBG cause?

A

Increased total T4

Normal fT4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does decreased TBG cause?

A

Reduced total T4

Normal fT4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How do T3 and T4 increase the basal metabolic rate?

A

Increase the number and size of mitochondria
Increase oxygen use and ATP hydrolysis
Increase synthesis of respiratory chain enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How much of thermogenesis do T3 and T4 contribute to?

A

~30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What effects do T3 and T4 have on carbohydrate metabolism?

A

Increase blood glucose:
- Stimulate glyogenolysis + gluconeogenesis
Increase insulin-dependent glucose uptake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What effects do T3 and T4 have on lipid metabolism?

A

Mobilise fats from adipose

Increase fatty acid oxidation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What effects do T3 and T4 have on protein metabolism?

A

Increase protein synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What effects do T3 and T4 have on growth?

A

GHRH production and secretion requires T3 and T4
Permissive actions:
- Glucocorticoid-induced GHRH release
- Allows GH and somatomedin activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What effects do T3 and T4 have on the foetal and neonatal brain?

A

Myelinogenesis

Axonal growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How do changes in T3 and T4 concentrations affect the CNS?

A 
Hypothyroid:
     - Slow intellectual functions
Hyperthyroid:
     - Nervousness
     - Hyperkinesis
     - Emotional lability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What affect does T3 and T4 have on the SNS?

A

Increases responsiveness to adrenaline and NA:
- By increasing the number of receptors
Also increases force and rate of heart contractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What happens to TRH in cold temperatures (in kids)?

A

TRH is released:

-> TSH released -> T3 and T4 release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What effect does stress have on thyroid hormone regulation?

A

Inhibits TRH and TSH release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

When are thyroid hormones highest and lowest?

A

Highest at night

Lowest in the morning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What family of 3 enzymes help activate and deactivate T3 and T4?

A

Deiodinase enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How do the deiodinase enzymes work?

A

Add/Remove an idoine atom in the outer ring of T3 and T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What enzyme activates T4 to T3 in tissues?

A

D2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Where is D1 found?

A

Liver

Kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Where is D2 found?

A

Heart and skeletal muscle
CNS
Fat
Thyroid and pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Where is D3 found?

A

Foetal tissue and placenta

Brain -> Except pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Weight gain, bradycardia, fatigue, cold intolerance, myxoedema (adults) and cretinism (kids) are signs of what?

A

Hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How does cretinism present?

A

Dwarfism

Reduced mental functioning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Why does thyroid-stimulating Ig cause Grave’s (hyperthyroidism)?

A

Acts like TSH:

 - Unchecked by T3 and T4
 - No negative feedback
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What causes exophthalmos in Grave’s?

A

Water-retaining carbohydrates build up behind eyes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What can a pituitary adenoma compress?

A

Optic chiasm -> Bitemporal hemianopia
CNs iii, iv and vi:
- iii -> Eye down and out
- iv -> Superior oblique paralysis -> Vertical diplopia
- vi -> Lateral rectus paralysis -> Horizontal diplopia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What else can a pituitary adenoma result in?

A 
Hypoadrenalism
Hypothyroidism
Hypogonadism
DI
GH deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are physiological causes of raised PRL?

A

Breast feeding
Pregnancy
Stress
Sleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What drugs can cause a raised PRL?

A

Dopamine antagonists (Metoclopramide)
Antipsychotics
Antidepressants (TCSa and SSRIs)
Others (Oestrogens and Cocaine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are pathological causes of a raised PRL?

A 
Hypothyroidism
Stalk lesions:
     - Iatrogenic
     - RTA
Prolactinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How do women present with a raised PRL?

A

Early
Galactorrhoea (30-80%)
Oligo-/Amenorrhoea
Infertility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How do men present with a raised PRL?

A 
Late
Impotence
Abnormal visual field
Headache
Anterior pituitary dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

In a patient with a raise PRL, what might we see in a pituitary MRI?

A

Micro-/Macroprolactinoma
Pituitary stalk lesion
Optic chiasm compression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

How is a prolactinoma treated?

A 
Dopamine agonists:
     - Bromocripton -> PO tds
     - Quinagolide -> PO od
     - Cabergoline -> PO twice weekly
               > Least side effects (most commonly used)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What causes acromegaly?

A

GH excess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What soft tissue features of acromegaly are there?

A

Thickened skin
Large jaw
Sweaty
Large hands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What cardiac features are present in acromegaly?

A

Hypertension

CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are some other features of acromegaly?

A 
Vascular headaches
Snoring/Sleep apnoea
DM
Mass effects:
     - Visual fields
Colonic polyps and cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How do we diagnose acromegaly?

A 
IGF-1:
     - Age and sex matched
Glucose tolerance test:
     - 75g PO suppression test
     - Check GH at 0, 30, 60, 90 and 120 minutes
     - Normal -> GH suppressed to
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What will the result of a glucose tolerance test be in a patient with acromegaly?

A

No suppression
Paradoxical rise
GH remains >1μg/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Why does glucose suppress GH?

A

GH stimulates an increase in blood glucose levels

So if glucose is raised, negative feedback will cause GH levels to drop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is the first line treatment for acromegaly?

A

Pituitary surgery

Followed by external radiotherapy to pituitary fossa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is the second line treatment and when is it commenced?

A 
Drug treatment:
     - Cabergolin
     - Octreotide (Somatostatin analogue)
     - Pegvisomat
If on GTT retest, GH is still >1μg/L
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

At what GH level is a patient clinical safe from further progression of acromegaly?

A

GH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What effects do somatostatin analogues have in acromegaly?

A 
Reduce GH in most
Shrink the tumour by 30-50%:
     - 6-12 months for effect
     - Recurs 6 weeks if stopped
Relieves headaches 1 hours post-op
Improve surgical outcomes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What are some side effects of somatostatin analogues?

A 
Local stinging
Short term:
     - Flatulence
     - Diarrhoea
     - Abdominal pain
Long term:
     - Gastritis (
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

How does pegvisomat work?

A

GH antagonist:

- Binds to GH receptor competitively

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

How is pegvisomat administered?

A

S/C injection:

- 10-30mg/dayy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What effects does pegvisomat have?

A

No decrease in tumour size
Reduces IGF-1
May increase serum GH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Why is pegvisomat the last line therapy?

A

20mg does costs £36000/year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What cancers must be screened for after acromegaly has been treated?

A

Colon

Tubulo-villous adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What CVS risk factors need monitored after acromegaly treatment?

A

BP
Lipids
Glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What regulates aldosterone?

A

RAAS

Plasma K+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What encourages the hypothalamus to increase CRH production and, hence, increase cortisol production?

A

Stress
Illness
Time of day (Peak at 9am)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

When is the RAAS activated?

A

When blood pressure falls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

How does angiotensin ii correct BP?

A

Directly by vasoconstriction
Indirectly via aldosterone:
- Increases Na+ reabsorption in kidney
- Hence water reabsorption increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What are the 6 classes of steroid receptors?

A 
Glucocorticoid
Mineralocorticoid
Progestin
Oestrogen
Androgen
Vitamin D
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What effect does cortisol have on the CVS?

A

Increases cardiac output
Increases BP
Increases renal blood flow -> Increases GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What effect does cortisol have on the CNS?

A

Mood lability
Euphoria
Decreased libido

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What effect does cortisol have on bone and connective tissue?

A

Increased rate of osteoporosis
Reduces serum calcium
Reduces collagen formation
Reduces wound healing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What effect does cortisol have on metabolism?

A

Increases blood glucose
Increases lipolysis
Increases proteolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What effect does cortisol have on the immune system?

A

Reduced capillary dilation
Reduced leucocyte migration
Reduced macrophage activity
Reduced cytokine production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What are the three main principles of using corticosteroids for clinical treatments?

A

Reduce inflammation -> Supraphysiological dose
Immunosuppression -> Supraphysiological dose
Replacement therapy -> Physiological dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Which administration route is better for corticosteroids; IM or IV?

A

IM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What are corticosteroids used to treat (mainly)?

A 
Allergy
Inflammatory disease:
     - RA
     - UC
     - Crohn's
Malignancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What effects does aldosterone have?

A

Na+/K+ balance:
- Increases Na+ reabsorption
- Increases K+/H+ secretion (and hence excretion)
Increases blood pressure:
- Water follows Na+ -> Increased water reabsorption
Regulates ECV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

In which of these locations are mineralocorticoid receptors not found:

  • Kidneys
  • Heart
  • Salivary glands
  • Gut
  • Sweat glands
A

Heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Where does primary adrenal insufficiency arise?

A

Adrenal gland

85
Q

What can cause primary adrenal insufficiency?

A

Addison’s
CAH
Adrenal TB/Malignancy

86
Q

What can cause secondary adrenal insufficiency?

A

Lack of ACTH
Exogenous steroid
Pituitary/Hypothalamic disorders

87
Q

What causes Addison’s Disease?

A

Autoimmune destruction of adrenal cortex

88
Q

True or false; Addison’s is the most common cause of adrenal insufficiency?

A

False
It is only the most common cause of primary adrenal insufficiency
Exogenous steroids are the most common cause overall

89
Q

What is Addison’s disease associated with?

A

T1DM
Thyroid disease (Grave’s)
Pernicious anaemia

90
Q

What are the clinical features of Addison’s disease?

A 
Weight loss
Fatigue
Hypotension -> Dizziness
GI:
     - Abdominal pain
     - Vomiting
     - Diarrhoea
Oligo-/Amenorrhoea
Skin pigmentation:
     - Skin creases
     - Buccal surfaces
91
Q

What biochemistry is seen in primary adrenal insufficiency:

  • CRH
  • ACTH
  • Cortisol
  • Aldosterone
  • Renin
  • Na+
  • K+
A 
CRH is high
ACTH is high
Cortisol is low
Aldosterone is low
Renin is high
Na+ is low
K+ is high
92
Q

What is the definitive diagnosis of primary adrenal insufficiency?

A 
Short synACTHen test:
     - Measure plasma cortisol
               > Before
               > 30 minutes after IV/IM ACTH
Normal result:
     - Baseline -> >250nmol/L
     - Post-ACTH -> >550nmol/L
Cortisol will barely rise on the synacthen test
93
Q

Should we delay treatment of adrenal insufficiency to confirm diagnosis?

A

NO

94
Q

How do we treat adrenal insufficiency?

A 
Hydrocortisone (cortisol replacement):
     - IV first if unwell
     - 15-30mg daily -> Divided doses
     - Mimic diurinal rhythm
               > 10 mg in the morning
               > 5mg at lunch and at night
Fludrocortisone (aldosterone replacement):
     - Monitor BP and K+
95
Q

What causes secondary adrenal insufficiency?

A

Lack of CRH and ACTH (hypothalamic disease) or ACTH (pituitary disease)

96
Q

What is the commonest cause of secondary adrenal insufficiency?

A

Exogenous steroids:

 - High dose prednisolone
 - Dexamethasone
 - Inhaled corticosteroid
97
Q

What are the clinical features of secondary adrenal insufficiency?

A

Similar to Addison’s:

 - Except no hyperpigmentation (since no ^ ACTH)
 - And aldosterone production is intact
98
Q

How is secondary adrenal insufficiency treated?

A

Hydrocortisone only

99
Q

What is Cushing’s syndrome?

A

Excess cortisol

100
Q

What are the clinical features of Cushing’s syndrome?

A 
Easy bruising
Facial plethora
Striae
Proximal myopathy
Central obesity
Acne
Amenorrhoea
Hypertension
Osteoporosis
101
Q

What are the ACTH-dependent causes of Cushing’s syndrome?

A 
Pituitary adenoma -> Cushing's DISEASE (68%)
Ectopic ACTH:
     - Carcinoid
     - Carcinoma (SCLC)
Ectopic CRH
102
Q

What are ACTH-independent causes of Cushing’s syndrome?

A 
Adrenal adenoma (10%)
Adrenal carcinoma (8%)
Nodular hyperplasia (1%)
103
Q

What causes primary Hypercortisolism/Primary Cushing’s syndrome?

A

Adrenal adenoma

104
Q

What causes secondary Cushing’s syndrome?

A

Pituitary adenoma (Cushing’s Disease)

105
Q

How can Cushing’s Syndrome be screened for?

A

Overnight dexamethasone suppression test
24hr urinary free cortisol
Late night salivary cortisol

106
Q

What is the definitive diagnostic test for Cushing’s Syndrome?

A

Low dose dexamethasone:

 - 0.6mg every 6 hours for 2 days
 - Repeat to confirm
107
Q

What is the commonest cause of cortisol excess?

A

Prolonged high dose steroid therapy:
- Chronic suppression of ACTH production
> Adrenal atrophy

108
Q

What is Conn’s syndrome?

A

Primary aldosteronism due to an adrenal adenoma

109
Q

What causes primary aldosteronism?

A

Autonomous production:
- Independent of Angiotensin ii and K+
Usually due to:
- Adrenal hyperplasia -> Bi-/Unilateral
- Adrenal adenoma -> Conn’s syndrome
- Familial

110
Q

True or false; Primary aldosteronism is the commonest secondary cause of hypertension?

A

True

111
Q

What are the clinical features of primary aldosteronism?

A

Significant hypertension
Hypokalaemia
Alkalosis

112
Q

What effects do aldosterone exert on the CVS?

A 
Increase cardiac collagen
Synthesis of:
     - Cytokines
     - ROS
Na+ retention
Altered endothelial function:
     - Increased pressure response
Increased SNS outflow
113
Q

What is the net effect of all the CVS functions of aldosterone?

A

Increased BP
LVH
Atheroma

114
Q

What is the commonest cause of primary aldosteronism?

A

Bilateral adrenal hyperplasia (60%)

115
Q

What percentage of primary aldosteronism cases are Conn’s syndrome (adrenal adenoma)?

A

30%

116
Q

In what conditions are K+ channel mutations seen?

A

Adrenal aldosterone-producing adenomas

Hereditary hypertension

117
Q

What is the function of the KCNJ5 channel and what happens if it is mutated?

A

Rectifying selective channel:
- Maintains membrane hyperpolarisation
Most mutations are gain-of-function and result in Na+ entry and depolarisation

118
Q

What is the first step in diagnosing primary aldosteronism?

A

Confirm aldosterone excess:
- Measure plasma aldosterone and renin
> Calculate aldosterone-renin ratio (ARR)
If ARR is raised:
- Saline suppression test
- Give 2L of saline
> Failure to suppress aldosterone by >50%
> Primary aldosteronism

119
Q

What is the second step in diagnosing primary aldosteronism?

A

Confirm subtype:

 - Adrenal CT -> Demonstrates adenoma
 - Adrenal vein sampling -> Confirms adenoma
120
Q

What surgical technique can be used to treat primary aldosteronism and when is it used? What does it cure?

A 
Unilateral laparoscopic adrenalectomy
Only if adrenal adenoma (confirmed on vein sampling)
Cures:
     - Hypokalaemia
     - 30-70% of hypertension
121
Q

When is medical treatment used in primary aldosteronism and what drugs are used?

A

In bilateral adrenal hyperplasia
Drugs:
- Spironolacton
- Eplerenone

122
Q

What is the commonest enzyme deficiency in CAH? What is the mode of inheritance

A

21-hydroxylase deficiency:

 - 1 in 120,000 live births
 - Autosomal recessive
123
Q

What is classical 21-hydroxylase deficiency?

A

Total deficiency
Salt-wasting
Simple virilising

124
Q

What is non-classical 21-hydroxylase deficiency?

A

Particl deficiency

Hyperandrogenaemia

125
Q

How is CAH diagnosed?

A

Basal/Stimulated 17-OH Progesterone will be very high:

 - >242nmol/L
 - Normal is
126
Q

Which of the following is not a presenting feature in males with classical CAH:

  • Presentation at 2-3 weeks old
  • Poor weight gain
  • Clear biochemistry
  • Acne
A

Acne

127
Q

What is the main presenting feature in females with classical CAH?

A

Ambiguous genitalie

128
Q

Which of the following is not a feature of non-classical CAH:

  • Hirsutism
  • Poor growth
  • Acne
  • Oligomenorrhoea
  • Precocious puberty
  • Infertility
A

Poor growth

129
Q

How is CAH treated in children?

A

Glucocorticoids
Mineralocorticoids
Surgery
Achieve maximum growth

130
Q

How is CAH treated in adults?

A

Control androgens
Restore fertility
Avoid steroid over-replacement

131
Q

What do the following clinical signs indicate:

  • Labile hypertension
  • Postural hypotension
  • Paroxysmal sweating
  • Headaches
  • Pallor
  • Tachycardia
A

Phaeochromocytoma

132
Q

What are some symptoms of phaeochromocytomas?

A 
Classical triad:
     - Hypertension
     - Headache
     - Sweating
Palpitations
SoB
Constipation
Anxiety
Weight loss
Flushing
133
Q

What complications can phaeochromocytomas cause?

A 
LVF
Myocardial necrosis
CVA
Shock
Paralytic ileus
134
Q

What happens to the following in phaeochromocytomas:

  • Glucose levels
  • Potassium
  • Haematocrit
  • Calcium
  • pH
A 
Hyperglycaemia
Hypokalaemia
Increased haematocrit
Mild hypercalcaemia
Lactic acidosis
135
Q

When should we investigate for phaeochromocytoma?

A 
FHx
Hypertension:
     - Resistant
     - If younger than 50
Classical symptoms
Hypertension + Hyperglycaemia
136
Q

How do we investigate phaeochromocytoma?

A

Confirm catecholamine excess:

 - Two 24hr urinary catecholamines
 - Plasma (At time of symptoms)
137
Q

How can we identify the source of the catecholamine excess?

A 
MRI:
     - Abdomen
     - Whole body
Meta-Iodobenzyguanidine (MIBG)
PET Scan
138
Q

How do we treat phaeochromocytoma medically?

A

Full α and β blockade:
- α before β
> If β done first -> Unopposed α-stimulation
-> Malignant arrhythmia
- Phenoxybenzamine (α-blocker)
- Propanolol/Atenolol/Metoprolol
Fluid/Blood replacement

139
Q

How do we treat phaeochromocytoma surgically?

A

Laparoscopic surgery:

 - Total excision
 - Tumour debulking
140
Q

What syndromes are phaeochromocytomas associated with?

A 
MEN2
Von-Hippel-Lindau Syndrome
Succinate Dehydrogenase mutations
Neurofibromatosis
Tuberose sclerosis
141
Q

What is the mode of inheritance of MEN2?

A

Autosomal dominant

142
Q

What causes MEN2?

A

Activating mutations in tyrosine kinase receptor:

- RET proto-oncogene

143
Q

What is MEN2 associated with?

A

Medullary thyroid cancer
Parathyroid hyperplasia
Bilateral phaeochromocytomas

144
Q

What causes Von-Hippel-Lindau Syndrome?

A

VHL gene mutations -> Autosomal dominant:

 - HIF protein accumulation
 - Cell proliferation
145
Q

What tumours does Von-Hippel-Lindau Syndrome tend to cause?

A

Haemangioblastomas (CNS + retina)
Endolymph tumours
Phaeochromocytomas/Paragangliomas

146
Q

What succinate dehydrogenase gene mutations can cause phaeochromocytomasa?

A

Inactivating mutations in SDH B, C + D:

- Destabilises HIF-1α

147
Q

What do SDH-D mutations cause?

A

Head and neck paragangliomas

>70% penetrance

148
Q

What do SDH-B mutations cause?

A

Malignant paragangliomas

149
Q

What are catecholamines also raised in?

A

CHF

150
Q

What sort of secretion do catecholamines usually have?

A

Episodic:

- Normal levels in plasma and urine may vary

151
Q

What sort of tumours are less-efficient at catecholamine synthesis?

A

Malignant and extra adrenal:

- Dopamine > NA > Adrenaline

152
Q

What drugs can cause hypercalcaemia?

A

Vitamind D

Thiazides

153
Q

What granulomatous diseases can cause hypercalcaemia?

A

Sarcoidosis

TB

154
Q

What high calcium turnover diseases can result in hypercalcaemia?

A

Bedridden
Thyrotoxic
Paget’s

155
Q

What are the biochemical features of primary hyperparathyroidism?

A

Increased serum calcium
Increased/Inappropriately normal serum PTH
Increased urine calcium excretion

156
Q

What malignant mechanisms can result in hypercalcaemia?

A 
Metastatic bone destruction
PTHrp from solid tumours:
     - Squamous cell lung cancer
     - Breast cancer
Osteoclast activating factors
157
Q

How can we diagnose hypercalcaemia caused by malignancy?

A

Increased calcium and ALP
Xray/CT/MRI
Isotope bone scan

158
Q

What is the acute treatment of hypercalcaemia?

A

Fluids:
- Rehydrate -> 0.9% saline 4-6L/24hrs
Consider loop diuretics once rehydrated
Bisphosphonates:
- Single does -> Reduces calcium in 2-3 days
- Max effect at one week
Occasionally steroids:
- Prednisolone -> 40-60mg/day for sarcoidosis
Salmon calcitonin

159
Q

When is Cinacalcet used?

A

Tertiary hyperparathyroidism

Parathyroid cancer

160
Q

What are indications for parathyroidectomy?

A 
End organ damage:
     - Bone disease
               > Osteitis Fibrosa Cystica
               > Brown tumours
               > Pepper pot skull (Multiple myeloma)
     - Gastric ulcers
     - Renal stones
     - Osteoporosis
Calcium >2.85mmol/L
Age
161
Q

What causes primary hyperparathyroidism? What biochemistry is seen?

A 
Primary parathyroid overactivity:
     - Adenoma
Biochemistry:
     - Raised PTH
     - Raised calcium
     - Normal renal function
162
Q

What causes secondary hyperparathyroidism? What biochemistry is seen?

A

Physiological response to hypocalcaemia
Biochemistry:
- Raised PTH
- Reduced calcium

163
Q

What causes tertiary hyperparathyroidism? What biochemistry is seen?

A 
Autonomous parathyroid activity after secondary
Biochemistry:
     - Raised PTH
     - Raised calcium
     - Other electrolytes skewed
164
Q

What inheritance does Hypocalciuric Hypercalcaemia have?

A

Autosomal dominant

165
Q

What mutations are present in Hypocalciuric Hypercalcaemia?

A

Deactivating mutations in Calcium-sensing receptor

166
Q

How is Hypocalciuric Hypercalcaemia diagnosed?

A

Mild hypercalcaemia
Reduced urinary calcium
PTH may be slightly raised
Genetic screening

167
Q

When does oogenesis begin?

A

In utero

168
Q

When does oogenesis restart after suspension?

A

Puberty

169
Q

When is oogenesis complete?

A

At fertilization

170
Q

When does oogenesis cease?

A

Menopause

171
Q

What are the primordial germ cells and what do they do?

A

Earliest recognisable female germinal cell
Capable of mitosis
Migrate to genital ridge by week 6 gestation

172
Q

What is oogonia?

A

Completion of last pre-meiotic division -> Oocytes

173
Q

When oocytes enter meoisis, what happens?

A

1st meiotic division -> Primary oocytes

2nd meiotic division -> Secondary oocytes

174
Q

What is the polar body?

A

First body is one of the two products in first stage of meiosis

175
Q

What does the presence of two polar bodies signify?

A

Sperm entry and completion of second meiotic division

176
Q

What happens during the follicular phase of the menstrual cycle?

A

Egg matures

Ready for oculation at midcycle

177
Q

What signifies the end of the follicular phase?

A

Ovulation

178
Q

What happens during the luteal phase of the menstrual cycle?

A

Development of corpus luteum

Induces preparation of reproductive tract for pregnancy

179
Q

What is the primary follicle?

A

Before birth, the primary oocyte is surrounded by a single layer of granulosa cells - Primary follicle

180
Q

How many primary follicles are there at birth and what is each capable of?

A

~2 million

Each can produce a single ovum

181
Q

What happens to the primary follicles until puberty?

A

Degenerate to scar tissue -> Atresia

182
Q

What is the secondary follicle?

A 
Oocyte grows (x1000) and follicle expands:
     - Differentiates under hormonal influence
183
Q

What happens to secondary follicles after puberty?

A 
~400 are ovulated
The rest (99.98%) undergo atresia
184
Q

What happens to follicular cells left behind after ovulation?

A

Undergo luteinisation:

- Become the corpus luteum

185
Q

What does the corpus luteum secrete and what is this important for?

A

Progesterone:

- Prepares uterine lining for implantation

186
Q

After ovulation, how long does the corpus luteum continue to grow?

A

8-9 days

187
Q

What is the maximum length of time the corpus luteum can survive without fertilisation?

A

14 days

188
Q

What does the corpus luteum do if fertilisation does occur?

A

Persists

Produces increasing amounts of progesterone (+oestrogen) until after pregnancy

189
Q

Where does FSH act and what does it do?

A

Acts on ovaries
Stimulates follicle development
Stimulates secretion of oestradiol
Stimulates ovulation

190
Q

Where does LH act and what does it do?

A 
Acts on ovaries
Stimulates:
     - Follicle maturation
     - Ovulation
     - Development of corpus luteum
     - Oestrogen secretion
191
Q

What happens during the follicular phase?

A
  1. Hypothalamus secretes GnRH
  2. Anterior pituitary secretes FSH + LH
  3. Up to 15 follicles are ‘rescued’ and begin to mature:
    • Granulosa and theca cells develop
192
Q

What do the theca cells produce?

A

Androgens

193
Q

What do the granulosa cells do?

A

Convert androgens to oestradiol by aromatase

194
Q

What does oestradiol to?

A

Thickens endometrium

Thins cervical mucus

195
Q

What does oestrogen do?

A

Suppresses FSH production:

- Selection of dominant follicle

196
Q

What does the granulosa in the dominant follicle express?

A

LH receptor

197
Q

What causes more GnRH release and when? What does this result in?

A

High oestrogen levels at the mid-cycle:

- Causes FSH + LH surge from anterior pituitary

198
Q

Put the following steps of ovulation in order:

  • Follicle wall weakens
  • LH + FSH levels fall
  • Cumulus oophorus loosens
  • Ovulation -> Oocyte, Zona Pellucida and cumulus
  • Inc in follicular fluid + number of granulosa
  • COC picked up by oviduct
A
  1. Inc in follicular fluid + number of granulosa
  2. Cumulus oophorus loosens
  3. Follicle wall weakens
  4. Ovulation -> Oocyte, Zona Pellucida and cumulus
  5. COC (cumulus-oocyte complex) picked up by oviduct
  6. LH + FSH levels fall
199
Q

What causes the corpus luteum to degenerate and what does it form?

A

At 12 days, if there is no hCG from an embryo the corpus luteum degenerates -> Corpus Albicans

200
Q

What is the function of hCG?

A

Maintains the corpus luteum

201
Q

When does the placenta take over progesterone production from the corpus luteum?

A

At 6 weeks gestation

Corpus luteum -> Corpus albicans

202
Q

What is the function of progesterone during pregnancy?

A

Supports pregnancy

Suppresses ovulation

203
Q

What role does FSH have in spermatogenesis?

A

Initiates spermatogenesis (with testosterone)
Causes Sertoli cells to express:
- Androgen Binding Globulin (ABG)
- Inhibin

204
Q

What role does FSH have in spermatocytogenesis?

A

Leads to development of Sertoli cells:

- Act as nursing cells for spermatids

205
Q

What role does LH have in spermatocytogenesis?

A

Promotes Leydig cell secretion of testosterone:

- Initiates spermatogenesis

206
Q

When does spermatocytogenesis occur?

A

In males at the age of puberty (10-14 years)

207
Q

What role does LH have in spermatogenesis?

A

Causes interstitial Leydig cells to secrete testosterone

208
Q

What role does testosterone have?

A 
Decreases release of:
     - GnRH
     - LH
Converted to dihydrotestosterone:
     - Enlargement of male sex organs
     - Secondary sexual characteristics
     - Anabolism
Binds to ABG made by Sertoli cells:
     - Increases its concentration in luminal fluid
               > Enables spermatogenesis
               > Enables sperm maturation in epididymis
209
Q

What does inhibin do?

A

Decreases secretion of FSH

Year 2 - Endocrinology (DP) (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions