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Phase 2a > Endo > Flashcards

Endo Flashcards

1
Q

are endocrine glands ducts or ductless?

A

ductless

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2
Q

exocrine ducts or ductless

A

ducts

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3
Q

paracrine v autocrine

A

paracrine -> nearby cells

autocrine -> own cell

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4
Q

water soluble hormones characteristics?

A

unbound
bind to surface receptors
short half life
fast clearance

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5
Q

water soluble hormones examples

A

peptide and monoamines

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6
Q

fat soluble characteristics?

A

proteins bound
diffuse into cells
long half life
cleared slowly

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7
Q

fat soluble hormones eg?

A

thyroid hormones and steroids

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8
Q

peptides characteristics?

A 
stored in secretory granules 
hydrophilic + water soluble 
released in pulses or burst
cleared by tissue or enzymes 
preprohormone -> prohormone -> hormone
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9
Q

insulin activation?

A

insulin binds to insulin receptors, this results in phosphorylation and activation of secondary messenger TYROSINE KINASE, cascade of effects and glucose uptake

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10
Q

process to get to adrenaline?

A

phenylalanine -> L-tyrosine -> L dopa -> dopamine -> nAd and Ad

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11
Q

what is noradrenaline broken down into and by?

A

Noradrenaline is broken down by Catechol-O-methyl transferase (COMT) into normetanephrine

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12
Q

what is adrenaline broken down into and by what?

A

Adrenaline is broken down by COMT into metanephrine

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13
Q

what is purpose of normetanephrine and metanephrine?

A

measured in serum - act as

indicators of noradrenaline or adrenaline activity

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14
Q

what is thyroid hormones bound to?

A

thyroid binding globulin

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15
Q

t3 v t4?

A

T3 - also known as Triiodothyronine - is more active
half life = 1 day
• T4 - also known as Thyroxine - less active but more produced
half life = 7 days

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16
Q

process of T3 and T4?

A

Incorporation of iodine on tyrosine molecule on thyroglobulin to form
iodothyrosines
• Conjugation of iodothyrosines gives rise to T3 and T4 and stored in
colloid bound to thyroglobulin
TSH stimulates the movement of colloid into secretory cell, T4 and T3
cleaved from thyroglobulin
• T4 can be thought of as a RESERVOIR for additional T3
• Majority of T3 is made from the breakdown of T4 → T3 which is
converted outside the thyroid gland

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17
Q

Vit D?

A
  • Fat soluble
  • Enters cell directly to bind to nucleus and stimulate mRNA production
  • Transported by vitamin D binding protein
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18
Q

steroids?

A
  • 95% protein bound
  • diffuse through plasma membrane
  • pass to nucleus to induce response
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19
Q

hormone receptor location for different hormones?

A

cell membrane for peptides
cytoplasm for steroids
nucleus for thyroid homoens, vit D and oestrogen

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20
Q

location of pituitary gland

A

Lies in a pocket of the sphenoid bone at the base of the brain, just below the
hypothalamus
• Sits in the pituitary fossa - just inferior to the OPTIC CHIASM - can get vision
problems e.g. hemianopia if there is acromegaly or pituitary tumour placing
pressure on the chiasm
• On either side lies the two cavernous sinuses - pathology in the pituitary can also affect the cavernous sinus structures

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21
Q

regulation of anterior pituitary by the hypothalamus?

A 
Stimulated to release
hypophysiotropic hormones by other areas of the CNS e.g. receptors that detect the outside
environment
• Secretes hypophysiotropic
hormones which reach the
anterior pituitary via the
HYPATHALAMO-HYPOPHYSEAL
PORATL VESSELS/VEINS and further stimulate the anterior pituitary to release 6 hormones
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22
Q

dopamine and prolactin

A

Prolactin is under negative control by dopamine thus if the pituitary
connecting stalk/infundibulum was destroyed then that would
results in an increase in the secretion of prolactin as its negative
pressure would not be able to reach it

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23
Q

does the anterior pituitary gland have arterial blood supply?

A

NO it receives blood through portal venous circulation from hypothalamus

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24
Q

FSH and LH; what they do?

A

Target the gonads
• Stimulate germ cel development (in females = ovum, in males = sperm)
• FSH stimulates oestrogen release
• Positive feedback is the release of oestrogen and stimulates LH
LH stimulates the release of the egg which in turn stimulates
progesterone release which results in increased thickening of the
uterine wall
• In men the effect of LH is on leydig cells resulting in testosterone release

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25
Q

Growth hormone; what it do?

A

Stimulates growth & protein synthesis
• Has effect on the whole body
• Stimulates glucogenesis and inhibits insulin resulting in an increase in
glucose
• Works on adipose tissue to break down fat
• Acts on liver to increase protein synthesis and stimulate IGF-1 which
acts on skeleton to increase cartilage proliferation
• IGF-1 is what is measured to reflect GH levels

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25
Q

Growth hormone; what it do?

A

Stimulates growth & protein synthesis
• Has effect on the whole body
• Stimulates glucogenesis and inhibits insulin resulting in an increase in
glucose
• Works on adipose tissue to break down fat
• Acts on liver to increase protein synthesis and stimulate IGF-1 which
acts on skeleton to increase cartilage proliferation
• IGF-1 is what is measured to reflect GH levels

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26
Q

ACTH, what it do?

A

• Stimulates the adrenal cortex to secrete CORTISOL from the zona
fasiculata
• Also stimulates androgen release from zona reticularis
• Also stimulate adrenaline release from adrenal medulla:
- Adrenaline is a major metabolic and stress hormone
• The effects cortisol are regulating and breaking down proteins, fats and
carbohydrates as well as an anti-inflammatory effect - lowered immune
response (if prolonged can be bad!!!)
• Most importantly, cortisol help the body overcome stress - without it we
would be unable to overcome stressful reaction - so risk of death e.g.
Addison’s disease

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27
Q

TSH; what it do?

A

Stimulates the release of thyroid hormone:

  • Controls rate of metabolic reactions
  • Accelerate food metabolism
  • Increases protein synthesis
  • Stimulation of carbohydrate metabolism
  • Increases ventilation rate
  • Increases cardiac output & heart rate
  • Brain development during foetal life and postnatal development
  • Growth rate acceleration
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28
Q

prolactin; what it do?

A

Stimulates the breasts to produce milk and helps with breast
development
• Inhibited by dopamine!

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29
Q

posterior pituitary gland difference?

A

Main difference is that hormone production is
ONLY in the hypothalamus and is then stored
in posterior pituitary

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30
Q

two hormones of posterior pituitary?

A

In the cell body of the supraoptic nucleus - VASOPRESSIN/ADH
- In the cell body of the paraventricular
nucleus - OXYTOCIN
short half life!

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31
Q

ADH?

A

Acts to decrease water secretion in the urine thereby retaining fluid in the
body and helping to maintain blood volume
Acts on smooth muscle cells around blood vessels to cause their
constriction resulting in vasoconstriction thereby increasing blood pressure
- this may occur in response to a decrease in blood pressure that resulted
from blood loss due to an injury
Also stimulates ACTH release from the anterior pituitary to increase
ALDOSTERONE release to further increase fluid retention!

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32
Q

Oxytocin?

A

Important for EJECTION of milk during breast feeding:
- The stimulation of mammary glands stimulates the release of
oxytocin and that stimulates the release of milk
• Pregnancy:
- Stimulates the contraction of uterine smooth muscles until the
baby is born
- Promotes the onset of labour - important for contractions!

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33
Q

diseases of pituitary?

A
  • benign pituitary ademona
  • craniopharyngioma
  • trauma
  • sheenas - pituitary infarction after labour
  • Sarcoid/TB
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34
Q

3 main presentations of pituitary tumour?

A

1 - pressure on local structures eg bitemporal hemianopia, hydrocephalus or CSF leak
2- pressure on normal pituitary causing HYPOPITUIRARISM eg, cortisol deficiency, central obesity, sallow complexion
3 - functioning tumour HYPERPITUITARISM eg, prolactimona (amenorhoea - treatement is CABERGOLINE which is a dopamine agonist), acromegaly due to increased GH and Cushing syndrome.

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35
Q

Diabetes mellitus definition?

A

Syndrome of chronic hyperglycaemia due to relative insulin deficiency,
resistance or both

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36
Q

normal glucose levels?

A

Blood glucose levels should be between 3.5-8.0mmol/L under all conditions

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37
Q

what does liver do in glucose homeostasis

A

Stores & absorbs glucose as glycogen - in post-absorptive state
• Performs gluconeogenesis from fat, protein and glycogen
• If blood glucose is HIGH then the liver will make glycogen (convert
glucose to glycogen) in a process called glycogenesis - in the long term
the liver will make triglycerides (lipogenesis)
• If blood glucose is LOW then the liver will split glycogen (convert
glycogen to glucose) in process called glycogenolysis - in the longer
term the liver will make glucose (gluconeogenesis) from amino acids/
lactate

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38
Q

what is the major consumer of glucose

A

BRAIN
This is because the brain CANNOT use free fatty acids to be converted to
ketones which can then be converted to Acetyl-CoA and used in the Kreb’s
cycle for energy production, since free fatty acids CANNOT CROSS the
BLOOD BRAIN BARRIER

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39
Q

what insulin do?

A

Suppresses hepatic glucose output - decreases glycogenolysis &
gluconeogenesis
• Increases glucose uptake into insulin sensitive tissues:
- Muscle - glycogen & protein synthesis
- Fat - fatty acid synthesis
Suppresses:
• Lipolysis
• Breakdown of muscles (decreased ketogenesis)

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40
Q

biphasic insulin release?

A

B-cells can sense the rising glucose levels and aim to metabolise it
by releasing insulin - glucose levels are the major controlling factor
in insulin release
- First phase response is the RAPID RELEASE of stored insulin
- If glucose levels remain high then the second phase is initiated, this
takes longer than the first phase due to the fact that more insulin
must be synthesised

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41
Q

glucagon?

A

Increases hepatic glucose output - increases glycogenolysis &
gluconeogenesis
• Reduces peripheral glucose uptake
Stimulates:
- Lipolysis
- Muscle glycogenolysis & breakdown (increased ketogenesis)
- also gets help from adrenaline, cortisol and GH

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42
Q

which chromosome is insulin coded from?

A

11

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43
Q

formation of insulin.

A
  • precursor is proinsulin
  • c peptide joins the alpha and beta chains
  • the proinsulin is cleaved from C peptide and used to make insulin
  • this is packaged into insulin secreting granules
  • insulin then enters portal circulation where 50% of it is extracted and degraded in the liver
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44
Q

GLUT 1

A

Enables basal NON-INSULIN-STIMULATED glucose uptake into many
cells

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45
Q

GLUT 2

A

Found in BETA-CELLS of the pancreas
• Transports glucose into the beta-cell - enables these cells the SENSE
GLUCOSE LEVELS
• Is a low affinity transporter that is, it only allows glucose in when there is
a high concentration of glucose i.e. when glucose levels are high and
thus WANT insulin release
• In this way via GLUT2 beta-cells are able to detect high glucose levels
and thus release INSULIN in response
• Also found in the renal tubules and hepatocytes

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45
Q

GLUT 2

A

Found in BETA-CELLS of the pancreas
• Transports glucose into the beta-cell - enables these cells the SENSE
GLUCOSE LEVELS
• Is a low affinity transporter that is, it only allows glucose in when there is
a high concentration of glucose i.e. when glucose levels are high and
thus WANT insulin release
• In this way via GLUT2 beta-cells are able to detect high glucose levels
and thus release INSULIN in response
• Also found in the renal tubules and hepatocytes

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46
Q

GLUT 3

A

Enables NON-INSULIN-MEDIATED glucose uptake into BRAIN

NEURONES & PLACENTA

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47
Q

GLU 4

A

Mediates much of the PERIPHERAL ACTION of INSULIN
• It is the channel through which glucose is taken up into MUSCLE and
ADIPOSE TISSUE cells following stimulation of the insulin receptor by
INSULIN binding to it

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48
Q

insulin receptor

A

This is a glycoprotein, coded for on the short arm of chromosome 19, which
straddles the cell membranes of many cells
- When insulin binds to the receptor it results in the activation of tyrosine
kinase and initiation of a cascade response - one consequence of which is
the migration of the GLUT-4 transporter to the cell surface and increased
transport of glucose into the cell

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49
Q

secondary diabetes example?

A

Pancreatic pathology e.g. total pancreatectomy, chronic pancreatitis,
haemochromatosis
• Endocrine disease e.g. acromegaly and Cushing’s disease
• Drug induced commonly by thiazide diuretics and corticosteroids
• Maturity onset diabetes of youth (MODY):
- Autosomal dominant form of type 2 diabetes - single gene defect
altering beta cell function
- Tends to present <25 yrs with a positive family history

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50
Q

cause of DMT1?

A

Disease of insulin deficiency usually caused by autoimmune destruction of beta-
cells of the pancreas

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51
Q

epidemiology of DMT1?

A

<30 yrs
increased in Northern Europeans
patient is usually lean

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52
Q

LADA?

A

latent autoimmune diabetes in adults

- difficult to differentiate from type 2 but patients are learner and have circulating islet antibodies

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53
Q

risk factor of DMT1?

A

family history - HLA-DR3-DQ2
associated with other autoimmune diseases eg, coeliac, Addisons, pernicious anaemia and autoimmune thyroid
can be due to environmental factors eg, diet, enterovirus (coxsackie B4), vit D deficiency

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54
Q

pathophysiology of DMT1?

A

Results from autoimmune destruction by autoantibodies of the pancreatic
insulin-secreting Beta cells in the Islets of Langerhans
- Causing insulin deficiency and thus the continued breakdown of liver
glycogen (producing glucose and ketones) leading to glycosuria and
ketonuria as more glucose is in the blood
- In skeletal muscle and fats there is impaired glucose clearance:

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55
Q

DKA risk

A

Results from a reduced supply of glucose (since there will be a
significant decline in circulating insulin) and an increase in fatty acid
oxidation (due to an increase in circulating glucagon)
• The increased production of Acetyl-CoA leads to ketone body
production that exceeds the ability of peripheral tissues to oxidise them.
Ketone bodies are relatively strong acids (pH 3.5), and their increase
lowers the pH of blood
• This acidification of the blood can have many consequences but most
critical is the fact that it IMPAIRS THE ABILITY OF HAEMOGLOBIN TO
BIND TO OXYGEN - note if a patient is in diabetic ketoacidosis, the excess
ketones in the blood will result in their BREATH SMELLING OF PEAR
DROPS (KETONES)
• As a result of excess fat breakdown and can result in patient becoming
acidotic, anorexic (weight loss) dehydrated leading to AKI and
hyperglycaemia and eventual death

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56
Q

DMT2 epidemiology?

A
  • south asian, African and Caribbean
  • > 30
  • overweight
  • most common in males
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57
Q

risk factor DMT2?

A
  • family history
  • increasing age
  • obesity
  • ethnicity
  • environment; low birth weight (poor nutrition) and glucose intolerance
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58
Q

pathophysiology of DMT2?

A

Abnormalities of insulin secretion manifest early in the course of DMT2
- An early sign is loss of the first phase of the normal biphasic response to
insulin
- Established DMT2 is associated with hypersecretion of insulin by a depleted
beta cell mass
Hyperglycaemia and lipid excess are toxic to beta cells (glucotoxicity) and
this is thought to result in further beta cell loss and further deterioration or
glucose homeostasis
- Circulating insulin levels are typically higher than in non-diabetics following
diagnosis and tend to rise further, only to decline again after months or years
due to eventual secretory failure - phenomenon is known as the Starling
curve of the pancreas

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59
Q

IGF AND IFG

A

type 2 progresses from impaired glucose tolerance IGF or impaired fasting glucose IFG and this is a window for lifestyle interventions to prevent full DMT2

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60
Q

IGT levels and IFG levels

A

IGT -> <7mmol/L

IFG -> more than 6.1 but less than 7

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61
Q

clinical presentations DMT1

A 
ACUTE
- leaner 
- more marked polydipsia, polyuria, weight loss and ketosis 
SUB ACUTE
- tiredness, visual blurring, balantis
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62
Q

clinical presentations DMT2?

A
  • central obesity
  • polydipsia, polyuria
  • acanthosis nigricans
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63
Q

diabetes diagnosis values?

A
  • Random plasma glucose > 11.1mmol/L = DIABETES DIAGNOSIS
    • Fasting plasma glucose > 7mmol/L = DIABETES DIAGNOSIS
  • For both tests one abnormal value is DIAGNOSTIC in symptomatic
    individuals
  • Two abnormal values are required in asymptomatic individuals
  • HbA1c > 6.5% normal (48mmol/mol) = DIABETES DIAGNOSIS
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64
Q

borderline diabetes diagnosis

A
  • OFTT fasting >7mmol

- 2hrs after glucose > 11.1

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65
Q

DMT1 treatments?

A

INSULIN

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66
Q

types of insulin treatments

A

short acting soluble
short acting insulin analogues
long acting insulin

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67
Q

short actin insulin analogues

A

Start working within 30-60 minutes and last for 4-6 hours
- Given 15-30 minutes before meals in patients on multiple dose regimens and by continuous IV infusion in labour, during medical
emergencies, at the time of surgery and in patients using insulin
pumps

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68
Q

short acting insulin analogies

A

Human insulin analogies (insulin aspart, insulin lispro, insulin
glulisine) have a fast onset and a short duration than the soluble
insulin but overall DO NOT IMPROVE DIABETIC CONTROL
- Have a reduced carry-over effect compared to soluble insulin and
are used with the evening meal in patients who are prone to
nocturnal hypoglycaemia

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69
Q

long acting insulin

A

Insulin premixed with retarding agents (either protamine or zinc)
precipitate crystals
- Can be intermediate (12-24 hrs) or long-acting (more than 24hrs)
- The protamine insulins are also known as isophane or NPH
insulins
- The zinc insulins are also known as lente insulins
- Insulin glargine is a structurally modified insulin that precipitates
in tissues and is then slowly released from the injection site

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70
Q

complication of insulin treatment?

A

Hypoglycaemia - most common (also caused by SULFONYLUREA)
• Injection site - lipohypertrophy
• Insulin resistance - mild and associated with obesity
• Weight gain - insulin makes people feel hungry

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71
Q

first line treatment for DMT2?

A
  • lifestyle advice
  • ACE inhibitors
  • statins
  • exercise
  • ORLISTAT - intestinal lipase inhibitor
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72
Q

second line treatment for DMT2?

A
  • biguanide -> metformin (reduces gluconeogenisis in liver, increases sensitivity to insulin and reduces CVS risk)
  • if HbA1c >53, 16 weeks later can give sulfonylurea eg, GLICLAZIDE which promotes insulin secretion but cannot be given in pregnancy and effects wears off as beta cell declines
  • at 6 months if HbA1c > 57 then ISOPHANE INSULINE (long acting analogue) or glitazone PIOGLITAZONE
  • alternative is sulfonylurea receptor binders NATEGLINDE
  • GLP analogues EXENATIDE which is an alternative to insulin
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73
Q

risk factors for DKA?

A

5 I’s

  • infection
  • insulin removal
  • infarction
  • infant - pregnancy
  • intoxication
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74
Q

clinical presentation of DKA?

A
  • dehydration
  • vomiting
  • drowsiness
  • sunken eyes
  • kussmauls respiration (deep breathing)
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75
Q

diagnosis of DKA?

A

Hyperglycaemia - blood glucose > 11mmol/L
- Raised plasma ketones > 3mmol/L - measured using a finger prick sample
and near-patient meter that measure Beta-hydroxybutyrate (major ketone)
- Acidaemia - blood pH < 7.3
- Metabolic acidosis with bicarbonate < 15mmol/L

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76
Q

treatment of DKA?

A
  • ABC
  • replace fluid with 0.9% saline
  • restore electrolyte loss
  • give insulin and glucose
  • monitor blood glucose and K+
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77
Q

hyperosmolar hyperglycaemic staete?

A

This is a life-threatening emergency characterised by marked hyperglycaemia,
hyperosmolality and mild or no ketosis
• This is the metabolic emergency characteristic of uncontrolled type 2 diabetes
mellitus

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78
Q

risk factors of HOHG state?

A

infections; pneumonia
assumption of glucose rich fluids
thiazide diuretics or steroids

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79
Q

pathophysiology of HOHG state?

A

Endogenous insulin levels are reduced but are still sufficient to inhibit
hepatic ketogenesis but insufficient to inhibit hepatic glucose production
risk of cerebral oedema due to hyperosmolality

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80
Q

clinical presentation of HOHG state?

A
  • dehydration
  • hyperglycaemia
  • syncope
  • no ketones in blood/urine
  • hyperosmolality
  • bicarb not lowered
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81
Q

diagnosis of HOHG state?

A

blood glucose > 11
high plasma osmolality
total K+ is low due to osmotic diuresis but serum K+ is raised due to absence of insulin

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82
Q

treatment of HOHG state?

A
  • low rate of insulin
  • fluid replacement 0.9%
  • low molecular weight heparin to reduce CVS risk
  • K+ restoration
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83
Q

pre-proliferative retinopathy?

A

• Micro-infarcts within the retina due to occluded vessels cause “cotton
wool spots” - this is a sign of retinal ischaemia and should be referred to
specialist

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84
Q

proliferative retinopathy?

A

Develops as a consequence of damage to retinal blood vessels and the
resultant retinal ischaemia
• Ischaemia results in the release of vascular growth factors (VEGF)
- some vessels are helpful but others haemorrhage and cause vision loss

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85
Q

maculopathy?

A

Fluid from leaking vessels is cleared poorly in the macular area
so when macula oedema occurs, it distorts and thickens retina causing central vision loss

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85
Q

maculopathy?

A

Fluid from leaking vessels is cleared poorly in the macular area
so when macula oedema occurs, it distorts and thickens retina causing central vision loss

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86
Q

hypoglycaemia diagnosis?

A

<3 mol of plasma glucose

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87
Q

aetiology of hypoglycaemia in non-diabetes?

A 
EXPLAIN
EX - exogenous drugs 
P - pituitary insufficiency 
L - liver
A - Addisons disease 
I - islet cell tumour 
N - non pancreatic neoplasm
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88
Q

clinical presentation of hypoglycaemia?

A

autonomic response; sweating, anxiety, tremor, palpations, dizziness
nueroglycopenic; confusion drowsiness, seizures, vision trouble

89
Q

diagnosis of hypoglycaemia with different markers?

A

if hypoglycaemic -? due to insulinoma
if low insulin, no excess ketones; due to non-pancreatic neoplasm or anti-insulin receptor antibodies
if low insulin and increased ketones -> alcohol, pituitary insufficiency or Addisons disease

90
Q

treatment for hypoglycaemia?

A
  • oral sugar and long acting start

- if NBM then 50% glucose IV or IM glucagon

91
Q

diabetes insipidus caused by?

A

decrease in ADH or lack of response to ADH

92
Q

types of diabetes insipidus?

A

nephrogenic and cranial

93
Q

diabetes insipidus differential?

A

primary polydipsia -> normal functioning ADH system but drinking excessive water leading to excessive urine production

94
Q

Nephrogenic Diabetes Insipidus aetiology?

A

nephrogenic diabetes insipidus is when the collecting ducts of the kidneys do not respond to ADH. It can also be caused by:

Drugs, particularly lithium used in bipolar affective disorder
Mutations in the AVPR2 gene on the X chromosome that codes for the ADH receptor
Intrinsic kidney disease
Electrolyte disturbance (hypokalaemia and hypercalcaemia)

95
Q

cranial diabetes insipidus aetiology?

A

Cranial diabetes insipidus is when the hypothalamus does not produce ADH for the pituitary gland to secrete. It can be idiopathic, without a clear cause or it can be caused by:

Brain tumours
Head injury
Brain malformations
Brain infections (meningitis, encephalitis and tuberculosis)
Brain surgery or radiotherapy
96
Q

presentation, diabetes insipidus?

A

polyuria, polydipsia, dehydration, hypernatraemia

97
Q

investigations, diabetes insipidus?

A

low urine osmolality
high serum osmolality
water deprevation test

98
Q

water deprivation test, method?

A

desmopressin test

  • patient doesn’t take any fluids for 8 hrs
  • urine osmolality measured
  • then synthetic ADH is given
  • urine osmolality measured again
99
Q

water deprivation test, results?

A

cranial DI, urine osmolality is low at first but when synthetic ADH is given, it rises
nephrogenic DI, urine osmolality is low even when synthetic ADH is given

100
Q

management of DI?

A

desmopressin

101
Q

where is thyroid gland?

A

anterior neck between C5-T1

vertebrae

102
Q

physiology of thyroid hormone production

A

Synthesis begins when circulating IODIDE is actively cotransported with Na+
ions across the basolateral membranes of the follicular cells - this is known as
IODIDE TRAPPING, the Na+ is pumped back out of the cells via Na+/K+-
ATPases
- The negatively charged iodide ions then diffuse to the apical membrane of the
follicular cells and are transported into the colloid
- The colloid of the follicles contains large amounts of a protein called
THYROGLOBULIN
- Once inside the colloid iodide is rapidly oxidised to IODINE which then bind
to TYROSINE RESIDUES on the thyroglobulin molecules by thyroid peroxidase
- tyrosine + 1 iodine = t1
- tyrosine - 2 iodine = t2
- When the thyroid is STIMULATED to produce thyroid hormone, the T1 and T2 molecules are cleaved from their tyrosine backbone (but are still attached to
the thyroglobulin) and join to create T3 (T1 + T2) or T4 (T2 + T2
- PROTEOLYSIS of the thyroglobulin results in the release of T3 & T4 which
then are able to diffuse out of the follicular cells into the interstitial fluid and
from there into the blood

103
Q

is thyroid disease more common in male or female

A

FEMALE

104
Q

prevalence of hyperthyroidism and hypothyroidism

A 
hyper = 2.5%
hypo = 5%
105
Q

goitre?

A
  • A swelling of the thyroid gland that causes a palpable lump to form in
    the front of the neck
  • Mechanism is caused by TSH receptor stimulation which causes the
    thyroid to GROW IN SIZE
  • caused by hypo (pituitary detects low thyroid levels, producing more TSH causing thyroid enlargement) and hyperthyroidism (eg, in graves there is excess stimulation of TSH receptor which causes thyroid to procure more hormone and grow larger)
106
Q

diffuse goitre?

A

the entire thyroid gland swells and feels smooth to the touch.
eg, Graves and Hashimoto

107
Q

nodular goitre?

A

where solid or fluid-filled lumps called nodules develop within the thyroid and make the thyroid gland feel lumpy to touch
eg, adenoma or carcinomas

108
Q

thyrotoxicosis?

A

excess thyroid hormone in blood

109
Q

hyperthyroidism, epidemiology?

A

2-5% of all women at some time

20-40 yrs

110
Q

aetiology of hyperthyroidism?

A
  • graves disease
  • genetics, HLA B8
  • E.coli and gram - organisms contain TSH binding sites
  • stress
  • smoking
  • high iodine intake
  • other autoimmune diseases eg, vitiligo, Addisons, myasthenia gravis
111
Q

pathophysiology of hyperthyroidism?

A
  • Serum IgG antibodies, specific for Graves’ disease, known as TSH
    receptor stimulating antibodies (TSHR-Ab) bind to TSH receptors
    in the thyroid
  • Thereby stimulating thyroid hormone production (T3 & T4) -
    essentially they behave like TSH
  • Resulting in excess secretion of thyroid hormones and
    hyperplasia of thyroid follicular cells resulting in hyperthyroidism
    and diffuse goitre
112
Q

clinical presentation of hyperthyroidism?

A
  • retro-orbital inflammation and swelling of extrocular muscles
  • exophthalmos - protruding eye
  • palpations
  • weight loss
  • oligomenorrhoea -> infrequent periods
  • tremor
113
Q

toxic multinoduar goitre?

A

Nodules that secrete thyroid hormones
• Seen in elderly and in iodine-deficient areas
• Commonly occurs in older women and drug therapy rarely produces
prolonged remission

114
Q

solitary toxic ademona/nodule?

A

Cause of about 5% of cases of hyperthyroidism

• Prolonged remission is rarely induced by drug therapy

115
Q

DE QUERVAINS’S THYROIDITIS:

A
  • Transient hyperthyroidism sometimes results from acute inflammation of
    the thyroid gland, probably due to viral infection
  • Usually accompanied by fever, malaise and pain in the neck
    • Treat with aspirin and only give prednisolone for severely symptomatic
    cases
116
Q

hyperthyroidism, drug induced?

A

AMIODARONE - anti-arrhythmic drug:
- Can cause both hyperthyroidism (due to the high iodine content of
amiodarone) and hypothyroidism (since it also inhibits the
conversion of T4 to T3)

117
Q

how to diagnose hyperthyroidism?

A
  • TFTs
  • TSH levels would be low due to negative feedback
  • T4 and T3 would be raised
  • in secondary hyperthyroidism, TSH would be elevated
  • TPO and thyroglobulin antibodies present in graves
118
Q

treatment of hyperthyroidism?

A
  • beta blockers PROPRANOLOL for symptoms
  • PROPYLTHIOURACIL stops conversion of T4 -> T3
  • ORAL CARBIMAZOL blocks thyroid hormone biosynthesis and has immunosuppressive effects (if given carbimazol, should give thyroxine to stop risk of hypothyroidism)
  • radioactive Iodine
  • surgery
119
Q

hypothyroidism - autoimmune?

A

The most common cause of hypothyroidism
• Associated with antithyroid autoantibodies leading to lymphoid
infiltration of the gland and eventual atrophy and fibrosis - since there is
atrophy there is NO GOITRE
• More common in FEMALES than males
• Incidence increases with age
• Associated with other autoimmune disease e.g. pernicious anaemia and
vitiligo

120
Q

Hashimoto thyroditis?

A

Produces atrophic changes with regeneration that results in GOITRE
FORMATION due to lymphocytic and plasma cell infiltration
• Gland is usually firm and rubbery but may range from soft to hard
• Thyroid peroxidase is an enzyme essential for the production and
storage of thyroid hormone
• Thyroid peroxidase antibodies (TPO-Ab) are present in HIGH TITRES
• Patients may be hypothyroid or euthyroid (normal thyroid function)
• LEVOTHYROXINE THERAPY may shrink the goitre, even when the
patient is not hypothyroid

121
Q

postpartum thyroiditis?

A

• Usually a transient phenomenon observed following pregnancy
• May cause hyperthyroidism, hypothyroidism or the two sequentially
• Thought to result from modifications to the immune system necessary in
pregnancy and histologically is a lymphocytes thyroiditis
(AUTOIMMUNE)
• Normally self-limiting but when conventional antibodies are found there
is a high chance of this proceeding to permanent hypothyroidism

122
Q

signs of hypothyroidism?

A 
BRADYCARDIC:
• Bradycardia
• Reflexes relax slowly
• Ataxia (cerebellar)
• Dry, thin hair/skin
• Yawning/drowsy/coma
• Cold hands +/- temperature drop
• Ascites
• Round puffy face
• Defeated demeanour
• Immobile +/- Ileus (temporary arrest of intestinal peristalsis)
• Congestive cardiac failure
123
Q

diagnosis of hypothyroidism?

A
  • TFTs
  • Serum TSH high (confirm primary hypothyroidism) - increases in an
    attempt to make thyroid work again
  • In secondary hypothyroidism the TSH is inappropriately low for
    the low T4/T3 - since issues is in the pituitary
    • Serum free T4 low - DIAGNOSTIC for HYPOTHYROID STATE
  • Thyroid antibodies and organ specific antibodies e.g. TPO-Ab (thyroid
    peroxidase antibody) in Hashimoto’s
    -
124
Q

treatment for hypothyroidism?

A
  • oral levothyroxine t4
125
Q

thyroid carcinoma types?

A
  • Papillary (70%):
    • Most common, well differentiated
    • Young people, local spread and good prognosis
    • Arise from thyroid epithelium
  • Follicular (20%):
    • Middle age, spread to lung/bone, usually good prognosis
    • Well differentiated, arise from thyroid epithelium
  • Anaplastic (<5%):
    • Very undifferentiated and arise from thyroid epithelium
    • Aggressive, local spread but poor prognosis
  • Lymphoma (2%):
  • Medullary cell (5%) - arise from calcitonin C cells of thyroid gland
126
Q

clinical presentation of thyroid carcinoma?

A
  • thyroid nodules

- dysphagia or horsiness

127
Q

thyroid carcinoma, treatment?

A
  • iodine (not for anaplastic carcinoma)
  • levothyroxine
  • chemo
  • surgery
128
Q

Cushing syndrome?

A

General term which refers to chronic excessive and inappropriate elevated
levels of circulating CORTISOL whatever the cause
- Alcohol excess mimics this

129
Q

cushings disease

A

Specifically refers to excess glucocorticoids resulting from inappropriate
ACTH (adrenocorticotrophic hormone) secretion from the pituitary due to
tumour

130
Q

epidemiology of Cushing syndrome?

A
  • people on oral steroids
  • alcohol intake
  • depression
  • obesity
  • pregnancy
131
Q

aetiology of Cushing syndrome?

A
  • Cushing disease most common -> bilateral adrenal hyperplasia from ACTH secreting pituitary ademoma
  • ectopic ACTH production from small cell lung cancer
  • ACTH independent (adrenal adenoma or from glucocorticoid use)
132
Q

pathophysiology of cushing syndrome?

A
  • Excess cortisol can either result from excess ACTH which in turn stimulates
    excess cortisol release or from neoplasms in the adrenals which in turn
    stimulate the zona reticularis to release more cortisol
  • Excess can also result from ingesting excess glucocorticoid itself e.g.
    PREDNISOLONE
133
Q

clinical presentation of Cushing syndrome?

A
  • moon face
  • central obesity
  • mood changes
  • gonadal dysfunction
  • muscle atrophy
  • purple striae
  • bruising
134
Q

differential diagnosis for Cushing syndrome?

A

pseudo-cushings from alcohol excess

135
Q

1st line investigations for Cushings syndrome?

A

Dexamethasone should, in the healthy patient, send negative feedback to
the pituitary and hypothalamus resulting in ↓ ACTH and thus reduced
cortisol
• Overnight dexamethasone suppression test:
- Oral dexamethasone 1mg at 00:00
- Measure serum cortisol at 8AM
- Normally there will be cortisol suppression < 50nmol/L
- In Cushing’s syndrome there will be no suppression
• Urine free cortisol over 24hrs is an alternative:
- Take > 2 measurements (cortisol is bound to albumin, when
capacity is reached then will spill out to urine)

136
Q

2nd line investigation for Cushing syndrome?

A

Perform 48hr dexamethasone suppression test:

  • Oral dexamethasone x4 a day for 2 days
  • Measure cortisol at 0hrs and 48hrs
  • In Cushing’s there will be no suppression of cortisol
  • can do ACTH test
  • if ACTH undetectable then could be due to adrenal tumour
  • If ACTH is detectable then is ectopic ACTH so either high dose dexamethasone suppression test of CRH test
  • if cortisol responds to CRH then Cushings disease if not, then ectopic ACTH production
137
Q

treatment for Cushing syndrome?

A
  • TSS
  • bilateral adrenalectomy but can cause nelsons syndrome (due to enlargement of pituitary tumour and causes skin pigmentation)
  • METYRAPONE, KETOCONAZOLE as they inhibit cortisone synthesis
138
Q

gigantism v acromegaly

A 
Gigantism:
- Excessive GH production in children BEFORE fusion of the epiphyses of the
long bones
Acromegaly:
- Excess GH in adults
139
Q

epidemiology of acromegaly?

A
  • equal in males and females

- >40 years

140
Q

aetiology of acromegaly?

A

Most cases are due to a benign GH-producing pituitary tumour
- In rare cases is due to hyperplasia e.g. ectopic GH-releasing hormone from
a carcinoid tumour

141
Q

risk factors of acromegaly?

A

5% are associated with MEN-1 (multiple endocrine neoplasia-1)

142
Q

pathophysiology of acromegaly?

A

-Increased GH either secreted due to pituitary tumour or due to ectopic
carcinoid tumour, travels to tissues such as the liver where it binds to
reporters resulting in an increase in IGF-1
- This stimulates skeletal and soft tissue growth giving rise to ‘giant-like’
appearance and symptoms
- Local tumour expansion in the pituitary can result in compression of
surrounding structures resulting in headaches & visual field loss

143
Q

clinical presentations of acromegaly?

A
  • skin darkening
  • coarsening face with wide nose
  • prognathism
  • big supraorbital ridge
  • fatigue
  • amenorrhea
  • decreased libido
144
Q

complications of acromegaly?

A
  • impaired glucose tolerance
  • sleep apnea
  • hypertension
  • CVS
145
Q

diagnosis of acromegaly?

A

Plasma GH levels:
• Can exclude acromegaly if random GH is undetectable or GH < 0.4 ng/
ml and there is normal IGF-1
• But a detectable value is NON-DIAGNOSTIC since:
- GH secretion is pulsatile
- GH increases in; stress, sleep, puberty and pregnancy
- If detected then proceed to glucose tolerance test (GTT)
- insulin like growth factor test

146
Q

treatment for acromegaly?

A

1st line -> TSS
2nd -> somatostatin analogues eg, OCTREOTIDE or LANREOTIDE, GH receptor agonists PEGVISOMANT or dopamine agonist CABERGOLINE

147
Q

prolactimona aetiology?

A

Prolactinoma:
• Tumour of pituitary result in excess prolactin release
• Can be micro or macro-adenoma
Pituitary stalk damage:
• Resulting in less dopamine so disinhibition of prolactin
• Due to pituitary adenomas, surgery or trauma
Drugs:
• Most common cause
• Metoclopramide or ecstasy
Physiological:
• Pregnancy, breast feeding, stress

148
Q

clinical presentations of prolactimona?

A
  • amenorrhoea
  • galactorrhea
  • low libido
  • headache
149
Q

diagnosis of prolactinoma

A

measure basal prolactin levels

150
Q

treatment of prolactinoma?

A

dopamine agonist - ORAL CABERGOLINE

151
Q

what is conns syndrome ?

A

Primary hyperaldosteronism:
- Excess production of aldosterone, independent of the renin-angiotensin
system
- Resulting in increased sodium and thus water retention (resulting in
increased BP), and decreased renin release

152
Q

aetiology of primary hyperaldosteronism?

A

2/3rds - Adrenal adenoma that secretes aldosterone - Conn’s syndrome
1/3rd - Bilateral adrenocortical hyperplasia

153
Q

pathophysiology of conns syndrome?

A

Disorder of the adrenal cortex characterised by excess aldosterone
production leading to Na+ and water retention and K+ loss (since need to
balance charge) and the combination of hypokalaemia and hypertension due
to aldosterone producing carcinoma (Conn’s) or adrenocortical hyperplasia

154
Q

clinical presentation of conns syndrome.

A
  • hypertension

- hypokalemia ->weakness, cramps, polyuria, polydipsia

155
Q

differential diagnosis to primary hyperaldosteronism?

A 
Must be differentiated from secondary hyperaldosteronism which arises where there is excess renin which stimulates
aldosterone release (its when BP in kidney > rest of the body so can be due to renal artery stenosis and heart failure)
156
Q

diagnosis of conns syndrome?

A
  • ECG -> hypokalaemia

- plasma aldosterone:renin ratio

157
Q

treatment for conns syndrome?

A

Laproscopic adrenalectomy
- Aldosterone antagonist e.g. ORAL SPIRONOLACTONE for 4 wks pre-op to
control BP and K+

158
Q

epidemiology of Addisons?

A

more in females

159
Q

Aetiology of Addisons?

A

1- Autoimmune adrenalitis - most common 80% of cases in UK:
• Destruction of the adrenal cortex by organ-specific antibodies, with 21-
hydroxylase as the common antigen
2- TB - common worldwide
3- adrenal metastases
4- long term steroid use
5- opportunistic infection in HIV eg CMV

160
Q

pathophysiology of Addisons?

A
  • Destruction of the entire adrenal cortex resulting in reduced glucocorticoid
    (cortisol), mineralocorticoid (aldosterone) and androgen production
  • All steroids are reduced which differs from hypothalamic-pituitary disease in
    which mineralocorticoid and androgen secretion remains largely intact due to
    their relative independence from the pituitary
  • In Addison’s the reduced cortisol levels lead, through feedback, to increased
    CRH and ACTH production, the latter being responsible for
    hyperpigmentation
161
Q

clinical presentation of Addisons?

A
  • lethargy
  • anorexia
  • vitiligo
  • tanned skin
  • postoral hypotension
  • tachycardia
162
Q

diagnosis of Addisons?

A

short ACTH test
Measure plasma cortisol before and 30 mins after IM TETRACOSACTIDE
(SynACTHen - ACTH analogue)
• Addison’s is excluded if 30 min cortisol > 550nmol/L

163
Q

treatment of Addisons?

A
  • IV HYDROCORTISONE, IV 0.9% SALINE AND GLUCOSE

- steroid therapy eg, ORAL HYRDOCORTISONE and ORAL FLUDROCTORISONE

164
Q

secondary hypoadrenalism?

A

no issue with adrenal glands but pituitary

165
Q

aetiology of 2nd hypoadrenalism?

A
  • iatrogenic is common cause

- rare is HPA disease

166
Q

pathophysiology of 2nd hypoadrenalism?

A

Causes result in a reduction in the release of ACTH resulting in decreased
glucocorticoid (CORTISOL)
- Mineralocorticoid production remains intact

167
Q

clinical presentation of 2nd hypoadrenalism?

A
  • vague symptoms of unwell

- NO SKIN HYPERPGMENTATION since acth is reduced

168
Q

treatment of 2nd hypoadrenalism?

A

ORAL HYRDROCORTISONE

169
Q

SIADH?

A

*Syndrome of inappropriate secretion of ADH**
Continues secretion of ADH despite of plasma being very dilute leading to
retention of water and excess blood volume and thus hyponatraemia (as Na+
becomes less concentrated)

170
Q

aetiology of SIADH?

A

tumour, pulmonary lesion, alcohol withdrawal, meningitis or drugs (chlopropamide -> sulfonylurea and carbamazepine)

171
Q

pathophysiology of SIADH?

A
  • Excess release of ADH will result in increased insertion of aquaporin 2
    channels in apical membrane of the collecting duct
  • This will result in excess water retention which in turn will dilute blood plasma
    thereby resulting in hyponatraemia as the Na+ concentration will decrease
172
Q

clinical presentations of SIADH?

A
  • anorexia
  • weakness
  • hyponatraemia
173
Q

diagnosis?

A
  • check Na+ which would be low
  • euvolaemia - normal blood volume
  • high urine Na+ >30
  • test with 1-2L of 0.9% saline and SIADH will not respond
174
Q

treatment of SIADH?

A
  • restrict fluid intake to increase Na+
  • if really symptomatic give hypertonic saline
  • can give oral demeclocyline which induces nephrpgenic DI
  • oral TOLVAPTAN - vasopressin antagonist but costly
175
Q

which is more common; hyper or hypocalcaemia?

A

hyper

176
Q

where is PTH secreted from?

A

chief cells in parathyroid glands

177
Q

what does PTH respond to?

A

decreased levels of ca2+

178
Q

actions of PTH?

A
  • Increasing osteoclastic resorption of bone - occurs rapidly
  • Increasing intestinal absorption of Ca2+ - slow response
  • Activation of 1,25-dihydroxyvitamin D (calcitriol) in the kidney
  • Increasing renal tubular reabsorption of Ca2+
  • Increasing excretion of phosphate
179
Q

how much total plasma of ca2+ is ionised?

A

40%

the rest is bound to albumin and unavailable to tissue

180
Q

VIt D hydroxylation?

A

Vitamin D is hydroxylated in the liver to 25-hydroxy vitamin D
25-hydroxy vitamin D then goes to the kidney where it is further
hydroxylated to 1,25-hydroxyvitamin D - known as calcitriol

181
Q

what is calciltrol stimulated by?

A

low plasma ca2+
low plasma phosphate
PTH

182
Q

what does cacitriol do?

A
  • Increased Ca2+ and phosphate absorption in the gut
  • Inhibits PTH release - negative feedback
  • Enhanced bone turnover by increasing numbers of osteoclasts
  • Increased Ca2+ and phosphate reabsorption in the kidney’s
183
Q

calcitonin?

A

made in c cells in thyroid

cause decrease in plasma ca2+ and phosphate

184
Q

HYERCALCAEMIA & HYPERPARATHYROIDISM: epidemiology?

A
  • Mild asymptomatic hypercalcaemia occurs 1 in 1000 of the population
  • Occurs especially in elderly women
  • Primary hyperparathyroidism and malignancies are by far the MOST
    COMMON CAUSES (90%) of hypercalcaemia
185
Q

primary hyperparathyoidism pathophysiology?

A

MOST COMMON CAUUSE
Generally of unknown cause
- 80% caused solitary by adenoma, 20% by hyperplasia of all glands
and < 0.5% due to parathyroid carcinoma
- Results in excess PTH production and thus hypercalcaemia
- Patient is most commonly asymptomatic
- symptoms are STONE, BONES, MOANS AND PSYCHIC GROANS
- high PTH
- high Ca2+
- low phosphate

186
Q

secondary hyperparathyroidism?

A 
Physiological compensatory hypertrophy of all parathyroids
resulting in excess PTH due to hypocalcaemia such that occurs in:
• Chronic kidney disease
• Vitamin D deficiency:
- Dietary
- GI disease e.g. Crohn’s
- Usually is asymptomatic in early stage
- Symptoms are predominantly bony
- PTH high
- Ca2+ low
- phosphate high (due to renal disease)
187
Q

tertiary hyperparthyroidism?

A

Occurs after many years of secondary hyperparathyroidism that
occurs from chronic kidney disease or vitamin D deficiency
- Causing glands to act autonomously having undergone hyper
plastic or adenomatous change resulting in excess PTH secretion
that is unlimited by feedback control
- Most often seen in CHRONIC RENAL FAILURE
- PTH high
- Ca2+ high
- phosphate high

188
Q

malignant hyperparathyroidism?

A

Parathyroid-related protein is produced by some squamous cell lung
cancer, breast and renal carcinomas:
- Mimic PTH resulting in hypercalcaemia
- PTH is low as the parathyroid-related protein is not detected

189
Q

what drugs can cause hypercalcemia?

A
  • thiazide diuretics
  • vit D analogues
  • lithium administration
190
Q

severe hypercalcaemia treatment?

A
  • Give bisphosphonates (to prevent bone resorption by inhibiting
    osteoclasts) after rehydration e.g. IV PAMIDRONATE
    • Measure serum U&E’s daily and serum Ca2+ 48hrs after initial treatment
    • Can give glucocorticoid steroids e.g. ORAL PREDNISOLONE in
    myeloma, sarcoidosis and vitamin D excess
191
Q

primary hyperparathyroidism treatment?

A

Parathyroid adenoma - surgical removal

- can give oral CINACALCET to increase sensitivity of parathyroid cells to ca2+

192
Q

hypocalcemia epidemiology?

A
  • Apparent hypocalcaemia may be an artefact of hypoalbuminaemia
  • Hypocalcaemia is extremely common in hospitalised patients and correlates
    with severity of illness - found in up to 88% of intensive care patients
193
Q

hypocaleamia aetiology?

A
  • CKD - most common
    Results from inadequate production of active vitamin D and renal
    phosphate retention - resulting in micro-precipitation of
    phosphate in the tissues
  • severe VITD deficiency
  • reduced PTH function - primary hypoparthyoidism due to autoimmune DiGeorge syndrome of idiopathic
  • secondary hypothyroidism following parathyroidectomy or thyroidectomy surgery
  • Pseudohypoparathyroidism -> failure of target cell response to PTH from mutation
  • Pseudopseudohypoparathyroidism -> inherited form father and very rare
194
Q

clinical presentations of hypocalcaemia?

A

SPASMODIC:
• Spasms - carpopedal spasms = Trousseau’s sign
• Perioral paraesthesia
• Anxious, irritable, irrational
• Seizures
• Muscle tone increases in smooth muscle hence wheeze
• Orientation impaired and confusion
• Dermatitis
• Impetigo herpetiformis - reduced Ca2+ and pustules in pregnancy
• Chvostek’s sign, Cataract, Cardiomyopathy

195
Q

diagnosis of hypocalcaemia?

A

hypo= PTH low, Ca2+ low and phosphate high
pseudo hypo = PTH high, Ca2+ low and phosphate high
pseudo pseudo = all normal

196
Q

treatment for acute hypocalceamia?

A

IV CALCIUM GLUCONATE over 30 mins with ECG monitoring

197
Q

vid D deficiency treatment?

A

ORAL COLECALCIFEROL

198
Q

hypoparathyroidism treatment?

A

calcium supplements + CALCITRIOL (active vitamin D)

199
Q

hyperkalaemia values?

A
  • Serum K+ > 5.5 mmol/L

• Serum K+ > 6.5mmol/L = MEDICAL EMERGENCY!

200
Q

epidemiology of hyperkalaemia?

A
  • Acute self-limiting hyperkalaemia occurs normally after vigorous exercise
    and is of no pathological significance
  • The most common causes are renal impairment and drug interference with
    K+ excretion
  • The combination of ACE-inhibitors with potassium sparing diuretics or
    NSAIDs is particularly dangerous:
201
Q

aetiology of hyperkalemia?

A
  • acute kidney injury
  • drugs; spironolactone, ramipril, NSAIDS, heparin, ciclosporin
  • Addisons disease
  • DKA
  • increased load
202
Q

pathophysiology of hyperkalaemia?

A

The amount K+ in the blood determines the excitability of nerve and muscle
cells, including the heart muscle or myocardium
- When K+ levels in the blood rise - this reduces the difference in electrical
potential between cardiac myocytes and outside of the cells meaning the
threshold for action potential is significantly decreased resulting in
increased abnormal action potential and thus abnormal heart rhythms that
can result in ventricular fibrillation and cardiac arrest

203
Q

clinical presentation of hyperkaleamia?

A
  • fast irregular pulse
  • chest pain
  • muscle weakness
  • kussmauls respiration
204
Q

differential diagnosis of hyperkalaemia?

A
  • leukaemia

- thrombocythaemia as K+ leaks out of platelets during clotting

205
Q

ECG hyperkalaemia?

A

Tall tented T waves, small P waves and wide QRS complex

206
Q

treatment for hyperkalaemia?

A

POLYSTYRENE SULFONATE RESIN which binds K+ in the gut and thus reduces absorption

URGENT K>7 give IV CALCIUM GLUCONATE - reduces the excitability of
cardiomyocytes

Give soluble insulin e.g. IV ACTRAPID - facilitates glucose uptake
into cell which brings K+ with it
- Must be accompanied by GLUCOSE to avoid hypoglycaemia
- IV or nebulised SALBUTAMOL - also drive K+ into cells

207
Q

hypokalaemia values?

A
  • Serum K+ < 3.5 mmol/L

• Serum K+ < 2.5 mmol/L = URGENT TREATMENT!

208
Q

epidemiology of hypokalaemia?

A
  • people taking diuretics
209
Q

aetiology of hypokalaemia?

A
  • increased renal excretion due to diuretics and hyperaldosterone
  • renal disease
  • GI loss; vomiting, diarrhoea
210
Q

clinical presentation of hypokalaemia?

A
  • muscle weakness
  • hypotonia
  • hyporeflexia
  • palpation
211
Q

ECG of hypokalaemia?

A

Small or inverted T waves, prominent U waves (after T waves), a long
PR interval, depressed ST segments

212
Q

treatment for hypokalaemia?

A

Mild - K+ > 2.5 mmol/L:
• Give oral K+ supplements e.g. ORAL SANDO-K
• If on thiazide diuretic and K+ > 3 mmol/L then consider a K+ sparing
diuretic e.g. SPIRONOLACTONE
- Severe - K+ < 2.5 mmol/L:
• IV K+ - but give cautiously and no more than 20mmol/h
• DO NOT GIVE K+ if oliguric (very small volume of urine output)
• NEVER give K+ as a fast stat bolus dose!!!

213
Q

carcinoid tumours/syndrome?

A

These tumours originate from the enterochromaffin cells (neural crest) and by
definition are capable of producing serotonin (5HT)

214
Q

what does serotonin do?

A

Bowel function

  • Mood
  • Clotting
  • Nausea
  • Bone density
  • Vasoconstriction
  • Increases force of contraction and heart rate
215
Q

what do carcinoid tumours secrete?

A

Bradykinin, tachykinin, substance P, gastrin, insulin, glucagon and
ACTH (thus Cushing’s)

216
Q

clinical presentation of carcinoid tumours?

A
  • spontaneous or induced blue-red flushing on face and neck caused by bradykinin release
  • RUQ pain
  • bronchoconstiction and broncospasm
  • diarrhoea
217
Q

carcinoid crisis?

A

When a tumour outgrows its blood supply or is handled too much
during surgery - mediators flow out
• There is LIFE-THREATENING:
- Vasodilation caused by bradykinin
- Hypotension - caused by ACTH which causes increased cortisol
- Tachycardia caused by serotonin
- Bronchoconstriction caused by bradykinin
- Hyperglycaemia caused by glucagon and ACTH

218
Q

treatment of carcinoid crisis?

A

high dose somatostatin analogue e.g. OCTREOTIDE

which reduces tumour hormone secretion

219
Q

differenital diagnosis to carcinoid syndorme?

A

Gastrointestinal stromal tumour (GIST):
• Mesenchymal tumours arising from interstitial Cajal cells (pacemakers for
gut contraction) of the wall of the gut
• Can co-exist with carcinoid tumours

220
Q

diagnosis of carcinoid tumours?

A

Ultrasound of liver:
• Confirms liver metastases
- Urine shows a high concentration of 5-hydroxyindoleacetic acid which is a
major metabolite of serotonin (5-HT)

221
Q

leptin function?

A

increases satiety and reduces hunger

222
Q

gherlin funciton

A

increases appetite and stimulates food intake

Phase 2a (12 decks)

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