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2a Bateman - Phase 2a MASTER DECK > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

WHAT IS ACROMEGALY?

What is it caused by?

https://www.youtube.com/watch?v=54h3IUbvHDU

A

Too much growth hormone from the pituitary gland

Tumour

or hyperplasia

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2
Q

What does the hypothalamus release? What does this cause? In acromegaly

A

Release growth hormone releasing hormone

Stimulates pituitary to release growth hormone

Somatostatin (growth hormone inhibiting hormone)
Decrease growth hormone release from pituitary

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3
Q

What do gigantism and acromegaly involve?

A

Increase in growth hormone

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4
Q

What is the difference between gigantism and acromegaly?

A

Difference in when growth hormone is released

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5
Q

When does gigantism occur?

A

Before the closure of the epiphyseal plates

End up very tall

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6
Q

When does acromegaly occur?

A

After epiphyses fuse

Not tall

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7
Q

At what age does acromegaly start?

A

At 20-40

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8
Q

What are the symptoms of acromegaly?

Go through each topic RS etc

A

RS
Snoring
GI
“Wonky bite” (malocclusion)
Int
↑Sweating
Endo
↑Weight
UG
↓libido; amenorrhoea
MSK
Arthralgia; backache
Neuro
Acroparaesthesia; headache

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9
Q

What are the signs of acromegaly?

A

Skin darkening
Acanthosis nigricans

Face
Big supraorbital ridge
Interdental separation
Macroglossia
Prognathism
Laryngeal dyspnoea

Spade-like hands and feet
Tight rings
Carpal tunnel syndrome

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10
Q

What are the complications of acromegaly?

A
  • *Impaired glucose tolerance** (40%)
  • *Diabetes Mellitus** (15%)

Vascular
HTN
LVH
Cardiomyopathy
Arrhythmias

Colon cancer

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11
Q

How can you diagnose acromegaly?

A

IGF-1 (somatomedin) tells tissues to grow
Elevated

Glucose tolerance test
75g or glucose
Wait 90 mins measure growth hormone levels
Will stay elevated! Should decrease

Growth hormone levels
Not usually used becaue pulsatile

CT or MRI
Could be no tumour, could be ectopic source

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12
Q

What is the treatment of acromegaly?

A

Trans-sphenoidal Surgery

Radiation

Medications - suppress GH
Somatostatin anaologues
Octreotide

Recombinant GH receptor antagonist
Pegvisomant

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13
Q

WHAT IS PROLACTINOMA?

A
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14
Q

WHAT IS CUSHING SYNDROME?

https://www.youtube.com/watch?v=ea1sXgd5ui8

A

Endocrine disorder with elevated cortisol levels in the blood

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15
Q

What is the cause of cushings DISEASE?

A

Pituitary adenoma making excess ACTH

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16
Q

What does the hypothalamus secrete in cushing’s?

A

Corticotropin releasing hormone

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17
Q

What does CRH stimulate?

A

Pituitary gland to release adrenocorticotropin hormone (ACTH)

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18
Q

What does ACTH do?

A

Affects cells in the adrenal cortex of the adrenal glands

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19
Q

What is the outer layer of the adrenal glands split into?

A

Zona glomerulosa

Zona fasiculata

Zona reticularis

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20
Q

What is the zona festiculata?

A

Largest zone

Stimulate cells in this zone to secrete cortisol

Cortisol is a glucocorticoids

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21
Q

What are glucocorticoids not?

What are they bound to?

How much is free in the blood?

A

Soluble in water

Cortisol-binding globulin

Only 5% free in blood

Less than that is active

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22
Q

What happens to excess free cortisol?

A

Filtered in kidneys and put into urine

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23
Q

What is free cortisol involved in?

(Type of cycle)

A

Part of circadian rhythm

High in moring

Low at night

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24
Q

So if there is a problem with cortisol levels what would this lead to?

A

Problems with circadian rhythm

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25
Q

What happens to cortisol during stress?

What does it do?

(type of process)

A

Increaes

Increase gluconeogenesis

Increase lipolysis

Increase proteolysis

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26
Q

How does cortisol maintain blood pressure?

A

Increase sensitivity of peripheral blood vessels to catecholamines

Adrenaline and noradrenaline

This narrows the blood vessel lumen

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27
Q

What does cortisol do to the immune response?

A

Decereases the production and release of inflamatory medaitors

Prostaglandins and interleukins

Inhibiting T-lymphcytes

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28
Q

What is cortisol involved with in the brain?

A

Mood and memory

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29
Q

How does the body keep control of cortisol?

A

Negative feedback mechanisms

Decrease production of CRH and ACTH

Less CRH causes less ACTH too

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30
Q

What does excess cortisol lead to?

Overload of what it normally reacts with

A

Severe muscle, bone and skin breakdown

Hypertension

Inhibit gonadotropin releasing hormone from hypothalamus

Dampens inflammatory response
More susceptible to infections

Impair normal brain function

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31
Q

What does elevated breakdown of muscle, bone and skin cause?

(What does this produce)

A

Elevated blood glucose

High insulin levels
Targets adipocytes in center of body
Activates lipoprotein lipase
Accumulate more fat molecules

Cause
Moon face
Buffalo neck hump

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32
Q

How is hypertension caused by excess cortisol?

A

Amplifies effect of catecholamines on blood vessels

Cortisol cross reacts with mineralcorticoid recptors

Mineralcorticoids released from zona glomerulosa

Triggers mineralcorticoid effect which is increasing blood pressure by retaining fluid

ALDOSTERONE

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33
Q

What does the inhibition of gonadotropin releasing hormone do?

A

Messes up ovarian and testicualr function

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34
Q

What are the causes of Cushing’s?

A

Exogenous cortisol
Medications (steroids)

Endogenous
Pituitary adenoma
Cushing disease
Cells don’t invade other tissues

Small cell lung cancer
ACTH

Tumour of the adrenal glands
Adrenal carciomas
Adrenal adenoma

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35
Q

Why do steroids cause Cushing’s?

A

Structure very similar to cortisol

Mimics action on tissue

Negative feedback on hypothamus and pituitary

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36
Q

How do the steroids affect the zona fesiculata?

A

Causes it to shrink in size

Because of lack of stimulation

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37
Q

How does a pituitary adenoma cause a rise in cortisol?

A

Causes the pituitary gland to secrete more ACTH

This affects the zona fasiculata

Causing it to grow in size

Secrete excess cortisol

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38
Q

What does a tumour on one adrenal gland do?

A

Divide abnormally and secrete excess cortisol

Suppress CRH and ACTH production

Other gland shrinks

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39
Q

What are the symptoms of Cushing’s?

A

Muscle wasting and thin extemities

Easy brusing

Abdominal striae

Fractues - osteoporisis

Full moon shaped face

Buffalo hump

Truncal obesity

Hypergylcemia
Diabetes mellitius
Hypertension
Cardiovascular disease risk
Increase vulnerability to infections
Poor wound healing
Amenorrhea
Psychiatric

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40
Q

What is the diangosis of Cushing’s?

A

ENDOGENOUS
Dexamethasone suppresion test
Low dose of dexamethasone (steroid)
Supressess ACTH production
Should cuase decrease cortisol levels

24 urine sample
Measuring free cortisol

Blood or saliva tests
Normal daily rise and fall of cortisol

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41
Q

What is the next stage after dexamethosone supression test?

A

ACTH plasma levels checked

Low ACTH gives diagnosis of
Adrenal adenomas and carcinoma

High ACTH gives diagnosis of
Cushing disease and ectopic ACTH production

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42
Q

What is the next stage if there is a high ACTH?

A

Injection of high amount of dexamethasone

Ectopic sites won’t respond

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43
Q

What types of imaging can be used?

A

MRI of pituitary

CT of adrenals

CT of chest abdomen or pelvis for ectopic

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44
Q

What is the treatment for Cushing’s?

A

Exogenous
Drug is gradually stopped
Adrenal crisis if too fast
Adrenal glands might be atrophied

Endogenous
Surgery
Adrenal steroid inhibitors
Ketoconazole and metyrapone
Most useful ectopic

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45
Q

What are you at risk of if you have your adrenals removed?

A

Nelson’s syndrome

Skin pigmentation increase

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46
Q

WHAT IS SYNDROME OF INAPPROPRIATE SECRETION OF ADH?

(Start with what it results in)

https://www.youtube.com/watch?v=0NHT8ERUBo0

A

Hyponatremia and hypo-osmolality

From inappropriate, continued secretion of ADH

Despite normal or increased plasma volume

Which results in impaired water excretion

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47
Q

What hormone controls water retention in the body?

What is it also called?

What does it also do?

A

ADH (vasopressin)

Also contricts arteries

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48
Q

What happens with the different levels of ADH?

A

More gives more water retention

Less gives less water retention

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49
Q

Where does ADH have its action on the nephron?

A

Distal convoluted and the collecting duct

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50
Q

What are the channels called that move into the membranes in the nepheron?

A

Aquaporins

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51
Q

What happens to the plasma osmolality when water is drunk?

A

Drops

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52
Q

What part of the body controls water regualtion?

A

Hypothalamus

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53
Q

What does the hypothalamus signal?

A

Pituitary

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54
Q

What does the pituitary do?

A

Decrease ADH

Less water retention

Increase osmolality

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55
Q

What happens if ADH continues to be secreted even if the plasma osmolality is low?

A

Increase aquaporins and increased water retention

Dilutes blood

Which dilutes sodium and also takes up more space

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56
Q

What does this taking up of more space cause to happen(hormone)?

A

Decrease aldosterone

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57
Q

What does the decrease in aldosterone do?

A

Excretes more sodium

This makes water follows

However end up with a very low sodium osmolality

Leading to SIADH

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58
Q

What are the different types of SIADH?

A

Type A

Type B

Type C

Type D

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59
Q

What is type A SIADH?

A

Erratic

Independent of plasma osmolality

Massive increase of ADH

Massive increase of urine osmolality

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60
Q

What is type B SIADH?

A

Constant release of ADH

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61
Q

What is type C of SIADH?

A

Baseline concentration of sodium is low

But is stable

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62
Q

What is type D SIADH?

A

ADH normal

Massive increase in urine osmolality

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63
Q

What are the symptoms caused by in SIADH?

A

Derived from decreased sodium in the blood

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64
Q

What are the symptoms of SIADH?

A

Dehydration

Headaches

Nausea

Vomiting

Muscle cramps

Cerebral oedema, Confusion, Mood swings

Seizure, Coma, Death

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65
Q

What is the diagnosis of SIADH?

A

Symptoms and lab results

Blood
Low sodium and low osmolality

Urine
High urine osmolality and high sodium

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66
Q

What causes SIADH?

A

Infection
Strokes
Haemorrhage
MS

Drugs
Mood stabilizers
Anti-epileptics

Surgery
Increased ADH secretion

Ectopic ADH
Small cell lung cancer

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67
Q

What is the treatment for SIADH?

A

Treat underlying cause

Restrict daily intake of fluid
High salt and protein diet

Inhibit ADH secretion drugs
Tolvaptan
Hypertonic IV fluids

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68
Q

THYROID DISORDERS?

A
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69
Q

What are the hormones produced by the thyroid gland?

A

Triiodothyronine (T3)
Active version x5 more

Thyroxine (T4)

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70
Q

What do the thyroid hormones do?

A

Burn foods

Stimulates sympathetic nervous system

GI motility

Increase heart rate

Increase blood pressure

Temperature

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71
Q

What does the hypothalamus release?

A

TRH

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72
Q

What does the pituitary release?

A

TSH

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73
Q

WHAT IS HYPOTHYROIDISM?

A

Low production of thyroid hormones

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74
Q

What is primary and secondary hypothyroidism?

A

Primary is a reduction in thyroxin (T4)

Secondary is a reduction in TSH

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75
Q

What are the causes of primary hypothyroidism?

A

Primary atrophic hypothyroidism (No goitre)

Hashimoto’s thyroiditis (Goitre)

Iodine deficiency

Post-thyroidectomy / radioiodine / antithyroid drugs

Lithium / amiodarone

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76
Q

What are the causes of secondary hypothyroidism?

A

Hypopituitarism

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77
Q

WHAT IS HASHIMOTO’s THYROIDITIS?

(inside hypothyroidism)

A

Autoimmune disease

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78
Q

What are the antibodies in hashimoto’s thyroiditis?

A

TRAbs = TSH receptor antibodies

Anti-Tg = Thyroglobulilin antibodies

TPOAb = Thyroperoxidase antibodies

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79
Q

What is the epidemology of hashimoto’s thyroiditis?

A

Older Women

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80
Q

What are the symptoms of hypothyroidism?

A

RS
Hoarse voice
GI
Constipation
Int
Cold intolerance
Endo
Weight gain
UG
Menorrhagia
MSK
Myalgia, weakness
Neuro / Psych
Tired, low mood, dementia

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81
Q

What are the signs of hypothyroidism?

A
  • *B**radycardic
  • *R**eflexes relax slowly
  • *A**taxia (cerebellar)
  • *D**ry, thin hair / skin
  • *Y**awning / drowsy / coma
  • *C**old hands +/- ↓T°C
  • *A**scites
  • *R**ound puffy face
  • *D**efeated demeanour
  • *I**mmobile +/- Ileus
  • *C**CF
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82
Q

What are the investigations for hypothyroidism?

A

TFT
TSH RAISED

Lipids/cholesterol
High

FBC
Macrocytosis

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83
Q

What are the associations of hypothyroidism?

A

AUTOIMMUNE
Type 1 Diabetes Mellitus
Addison’s disease
Pernicious anaemia
Primary biliary cirrhosis

INHERITED
Turner’s syndrome
Down’s syndrome
Cystic fibrosis

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84
Q

What is the treatment of hypothyroidism?

A

Levothyroxine (T4)

Higher doses in the young

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85
Q

WHAT IS HYPERTHYROIDISM?

A

Too much thyroid hormones

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86
Q

What are the causes of hyperthyroidism?

A

GRAVES’ DISEASE

TOXIC MULTINODULAR GOITRE

TOXIC ADENOMA

ECTOPIC THYROID TISSUE (mets / struma ovarii)

EXOGENOUS (Iodine / T4 excess)

DE QUERVAIN’S THYROIDITIS (post-viral)

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87
Q

What happens in graves disease?

What are the triggers?

A

Autoimmune

IgG autoantibodies bind to and stimulate TSH receptors

Infection, stress, childbirth

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88
Q

What are the classic symptoms of graves disease?

A

Eye disease, pretibial myxoedema, thyroid acropachy

Autoimmune (vitiligo, type 1 DM, Addison’s)

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89
Q

What are the symptoms of hyperthyroidism?

A

CVS
Palpitations
GI
Diarrhoea
Int
Heat intolerance
Endo
↓Weight, ↑appetite
UG
Oligomenorrhoea +/- infertility
Neuro / Psych
Tremor, irritability, labile emotions

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90
Q

What are the signs of hyperthyroidism?

A

HANDS
Palmar erythema; warm, moist skin; fine tremor

PULSE
Tachycardia; SVT; AF

FACE
Thin hair; lid lag / retraction

NECK
Goitre; nodules; bruit

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91
Q

What are the investigations for hyperthyroidism?

A

TFT
Increase T4 and T4

FBC
Normocytic anaemia

ESR (↑)

Calcium (↑)

LFT (↑)

Thyroid autoantibodies

Visual fields, acuity, eye movements

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92
Q

What is the treatment for hyperthyroidism?

A

β-blockers
Propanolol(rapid control of symptoms)

Antithyroid medication
Carbimazole SE = AGRANULOCYTOSIS
Block and replace (carbimazole + thyroxine)

Radioiodine (131I)

Thyroidectomy

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93
Q

What are some causes of goitre?

A

Physiological

Graves’ disease

Hashimoto’s thyroiditis

De Quervain’s

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94
Q

What are the thyroid cancers?

A

Papillary (60%)

Follicular (≤25%)

Medullary (5%)

Lymphoma (5%)

Anaplastic

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5
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95
Q

WHAT IS PRIMARY ADRENAL INSUFFIENCY?

https://www.youtube.com/watch?v=V6XcBp8EV7Q

A

The adrenal glands can’t produce enough hormones

Aldosterone and cortisol

Primary refers to the adrenal glands themselves

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96
Q

What can addison’s disease be?

A

Acute and chronic

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97
Q

What are the different layers of the adrenal glands?

A

Cortex
Zona glomerulosa
Zona fasiculata
Zona reticularis

Medulla

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98
Q

What does the zona glomerulosa produce?

A

Aldosterone

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99
Q

What does the renin, angiotensin aldosterone system do?

A

Decrease potassium

Increase sodium

Increase blood volume and pressure

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100
Q

What is aldosterone stimulate by?

A

Renin

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101
Q

What is aldosterones actions?

A

Bind to receptors on the distal convulted tubules

Sodium potassium ion pumps of principal cells
Work harder
Drive potassium into cell from blood
Flows down concentration gradient into urine
At same time sodium goes in the opposite direction
Water also moves into blood
Increasing blood pressure

Proton/ATP pumps in alpha-intercalated cells
More protons secreted into urine
Bicarbonate pumped into blood
Increases pH

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102
Q

What is produced in the zona fasiculata?

A

Cortisol and glucocorticoids

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103
Q

How is cortisol released?

A

Hypothalamus releasing corticotropin releasing hormone

Acts on pituitary

This releases adrenocorticotropin into blood

Acts on zona fasiculata

104
Q

What is special about cortisol?

A

Lipid soluble and can act on many cells in the body

105
Q

What is a function of cortisol?

A

Gluconeogensis

From muscle

and fat

106
Q

What does insulin do?

A

Reduce glucose levels in blood

107
Q

What does the zona reticularis do?

A

Make androgens

E.g. deyhydroepiandosterone

Precursor to testosterone

108
Q

What does testosterone do in males?

A

Contributes to development of male reproductive tissue

Secondary sex characteristics e.g. facial hair and adams apple

109
Q

What is testosterone do in females?

A

Growth spurt in development

Underarm and pubic hair during puberty

Increase sex drive in adulthood

110
Q

What is the production of androgens stimulated by?

A

ACTH

111
Q

What happens to the adrenal cortex in primary adrenal insufficiency?

A

Gets progressively damaged

112
Q

What are the causes of primary adrenal insuffiency?

A

In developed countries
Autoimmune destruction
Unclear reason

Developing countries
Tuberculosis
Infection spreads from lungs to adrenal glands

Metastatic carcinoma

113
Q

What does the adrenal cortex have which allows it to keep healthy?

A

High functional reserve

Allows it to keep up with small amount of cells present

114
Q

What do the symptoms of primary adrenal insufficiency depend on?

A

Which part of the adrenal cortex has been destroyed

115
Q

What happens if the zona glomerulosa is destroyed?

A

Aldosterone levels fall

Leads to high potassium levels in the blood

Low sodium - hyponatremia

Low sodium water moves out of the blood vessels
Hypovolemia

High protons in blood
Metabolic acidosis since it’s caused by the kidneys

116
Q

What are the symptoms if the zona glomerulosa is affected?

A

Cravings for salty foods

Nausea and vomiting

Fatigue

Dizzyness

117
Q

What happens if the zona fasiculata is destroyed?

A

Cortisol falls
Inadequate glucose levels in times of stress

Pituitary glands become overactive
Since usually cortisol has negative feedback on pituitary
Produces proopiomelinocortin
Precursor to ACTH and MSH

118
Q

What are the symptoms if the zona fasiculata is destroyed?

A

Fatigue in times of stress

Hyperpigmentation on knuckles and joints

119
Q

What happens if the zona reticularis is destroyed?

A

Men not affected

Testes major source of male androgens

Females
Loss of pubic hair
decreased sex drive

120
Q

What does primary adrenal insuffiency usually need to cause symptoms?

A

Symptoms often slow,

Major stressor comes along
Injury, surgery or infection
Cause symptoms to appear

Sudden need for aldosterone and cortisol

121
Q

What is it called when the body suddenly needs aldosterone or cortisol and the body can’t deliver?

A

Addisonian crisis (acute primary adrenal insufficiency)

122
Q

What are the symptoms of addisonian crisis?

A

Pain in back abdomen or legs

Vomiting and diarrhoea leading to dehydration

Low blood pressure leading to loss of consciousness

Death

123
Q

What syndrome can cause an addisonian crisis?

A

Waterhouse-friderichsen syndrome

Causes blood vessels in adrenal glands to rupture

124
Q

How can you diagnose addison’s disease?

A

ACTH hormone test
Small amount of synthetic ACTH injected
Measure cortisol and aldosterone produced
Both will be low

Bloods
FBC(anaemia, eosinophilia)
U&E(↓Na+, ↑K+, ↑Ca2+, ↑Urea)
BM(↓)

125
Q

What is the treatment for addison’s disease?

A

Homones

Cortisol
Aldosterone
Androgens

Take for life

Stopping can lead to crisis

126
Q

WHAT IS SECONDARY ADRENAL INSUFFICIENCY?

A

Lack of ACTH

and therefore cortisol

127
Q

What are the causes for secondary adrenal insufficiency?

A

Medications
Glucocorticoids

Pituitary mass or infection

128
Q

Why is aldosterone unaffected in secondary adrenal insufficiency?

A

Aldosterone secretion independent of ACTH

129
Q

What is the diagnosis of secondary adrenal insufficiency?

A

Bloods
Low cortisol

130
Q

What is the treatment for secondary adrenal insufficiency?

A

Glucocorticoid analogues

131
Q

WHAT IS CONN’S SYNDROME?

https://www.youtube.com/watch?v=JBfkGNr01V8&t=1s

A

Hyperaldosteronism

Adenoma of the glandular epithelial cells

Secrete too much aldosterone

132
Q

If there is high aldosterone levels, what will the ion levels be in the blood?

A

Potassium low

Sodium high

Less protons

133
Q

What do the ions in the blood in conn’s syndrome cause?

A

Hypertension

Metabolic alkolosis

134
Q

What are the symptoms of Conn’s syndrome?

A

Headaches and flushing

Constipation
Weakness
Heart rhythm changes

135
Q

What is the diagnosis of Conn’s syndrome?

A

Bloods
High levels of aldosterone
Low levels of renin

136
Q

What is the treatment for Conn’s syndrome?

A

Potassium sparing diuretic
Spirinolactone

Surgery
Remove tumour

137
Q

WHAT DIABETES MELLITUS?

A

Trouble moving glucose from blood into cells

High level in blood

Not alot in cells

138
Q

How does the body control movement of glucose in and out of cells?

A

Insulin
Decrease glucose

Glucagon
Increase glucose

139
Q

Where are the hormones released from to monitor blood glucose?

A

Islets of langerhans

Beta cells in the middle release insulin

Alpha cells on the periphery release glucagon

140
Q

What happens in a cell when insulin is released into the blood?

A

Insulin in the blood binds to receptors on muscle cells or adipose tissue

Causes vesicles containing glucose transporters to fuse with membrane

Allows glucose to enter

141
Q

What does glucagon do?

A

Causes the liver to make glucose from other sources

Breaks down glycogen into glucose

Put into blood

142
Q

What happens in diabetes mellitus?

A

Too much glucose in blood

143
Q

How much of the population has diabetes mellitus?

A

10%

144
Q

What are the different types of diabetes?

A

Type 1
10%

Type 2
90%

145
Q

What is type 1 diabetes mellitus?

A

Body doesn’t produce enough insulin

146
Q

What does the immune system do in type 1 diabetes and what type of hypersensitivity is it?

A

Bodies own cells attack the pancreas

Type 4 hypersensitivty reaction
Cell-mediated response

147
Q

What are antigens made up of?

A

Peptides

Polysaccarides

Lipids

148
Q

What is the process that gets rid of T cells which attack our own cells called?

A

Self tolerance

149
Q

What happens with type 1 diabetes which loses self tolerance?

A

Genetic abnormality

Loses self tolerance of T cells attacking beta cells

T cells attract other T cells

150
Q

What happens if beta cells are destoryed?

A

Glucose accumilates in blood

151
Q

What genes encode the MHCs?

What chromosome are they on?

A

HLA system

Chromosome 6

152
Q

Which genetic genes are affected in type 1 diabetes?

A

HLA-DR3

HLA-DR4

No everyone develops diabetes

153
Q

What are the symptoms of type 1 diabetes?

A

Polyphagia

Glycosuria

Polyuria

Polydipsia

154
Q

How does polyphagia happen?

A

Glucose can’t get into cells

Starved of glucose

Adipose tissue breaks down fat

Muscles break down protein

Causes weight loss and hunger

155
Q

How does glycosurina and polyuria happen?

A

Lots of glucose in blood goes into urine

Since glucose is osmotically active it draws water into it leading to polyuria

156
Q

How does polydipsia happens?

A

Since there is so much urination it leads to move drinking

157
Q

What are some complications of diabetics with bad control?

A

Vascular disease

Nephropathy

Neuropathy

Diabetic foot

Retinopathy

158
Q

What is the treatment for type 1 diabetes?

A

Lifelong insulin injections

Education

159
Q

What is a big complcation of type 1 diabetes?

A

Diabetic ketoacidosis

160
Q

What happens when the body breaks down fat?

A

Turns fat into fatty acids

161
Q

What does the liver turn the fatty acids into?

A

Ketone bodies

Acetoacitic acid
Ketoacid

Beta-hydroxybutyric acid
Reduced ketone

162
Q

What are ketone bodies used for?

A

Energy by cells

163
Q

What can ketones do to the blood?

A

Make the blood acidic

164
Q

What does making the blood acidic do to the body to compensate?

A

Kussmaul respiration

Deep/labored breathing
To reduce CO2
Reduce acidity

165
Q

What transporter to cells have on their surface?

A

Proton potassium transporter

166
Q

When there is no insulin what problem does this cause for cells?

A

Insulin also activates a potassium sodium pump

If there is none like in diabetes pump doesn’t work

More potassium stays outside of the cell

Gets into blood and causes hyperkalaemia

167
Q

What does the body do with all the potassium in the blood with diabetes?

A

Excretes it

But levels of potassium in cells stays low

168
Q

What is the high anion gap in diabetes?

A

Large measured difference in negative and positive ions

This is from ketoacid build up

169
Q

How can a diabetic ketoacidosis happen in somebody who already has insulin treatment?

A

A stress e.g. infection
Release of epinephrine
Release of glucagon
More glucose in blood
Loss of glucose in urine
Loss of water
Dehydration

Need for alternative energy
Generation of ketone bodies

170
Q

What do the ketone bodies break down into? What does this cause to the breath?

A

Acetone

Fruity smell

171
Q

What does ketoacidosis cause?

A

Nausea

Vomiting

Mental status changes

Cerebral oedema

172
Q

What is the treatment for diabetic ketoacidosis?

A

Fluids for dehydration

Insulin to lower blood glucose

Electrolytes (K+)

173
Q

What is type 2 diabetes mellitus?

A

Body makes insulin but the cells don’t respond

Not fully understood

174
Q

What happens when insulin gets to the cell?

A

Cells don’t respond

Transporters don’t go to the membrane

Insulin resistance

175
Q

What are the risk factors for type 2 diabetes?

A

Obesity

Lack of exercise

Hypertension

176
Q

What is thought to be a cause of diabetes type 2?

A

Excess of adipose tissue releases free fatty acids and adipokines

These two molecules can cause inflammation

This is related to insulin resistance

177
Q

What genetic factors show genetic link with diabetes type 2?

A

Having a twin with type 2 diabetes dramitically increases the risk of having diabetes in the twin

178
Q

What happens to the glands in the pancreas as a result of the cells not responding to insulin?

A

Secrete more insulin leading to beta cell hyperplasia and hypertrophy

179
Q

What is normoglycemia?

A

Insulin levels high when cells don’t respond to insulin

Blood glucose levels remain normal

180
Q

What other protein do the beta cells release?

A

Islet amyloid polypeptide (amylin)

181
Q

What happens in the beta cells of the pancreas after a while when they are trying to compensate?

A

Hypotrophy and hypoplasia

182
Q

What happens when the beta cells of the pancreas decrease?

A

Less insulin leading to hyperglycemia leading to polyuria etc etc

183
Q

What is different from type 1 diabetic ketoacidosis from type 2 diabetic ketoacidosis?

A

Insulin and glucagon balance is okay

so diabetic ketoacidosis doesn’t occur

184
Q

What is the state that is much more common in type 2 diabetes?

A

Hyperosmolar, hyperglycemic state

185
Q

What does hyperosmolar, hyperglycemic state cause?

A

Plasma osmolarity from dehydration

Increase concentration in glucose in blood

Sometimes mild ketoemia and acidosis

186
Q

What happens to the cells in HHS?

A

They shrivel up as water leaves them to go into the blood

187
Q

What does increased water in blood vessels do?

A

Lead to increased urination

and total body dehydration

188
Q

What does total body dehydration lead to?

A

Mental status changes

189
Q

What does HHS overlap with?

A

Diabetic ketoacidosis

190
Q

What are the test for diabetes?

A

Fasting glucose
No food or drink for 8 hours
7 mmol/l or over indicates diabetes

Non-fasting or random glucose
Over 11.1 mmol/l

Oral glucose tolerance
Over 11.1 mmol/l at 2 hours

HbA1C
Percentage or red blood cells with glucose on
48 or higher

191
Q

What is a complication of diabetes in blood vessels?

A

Cause damage to microvasculature

Hyalinearteriscleorsis

In capillaries basement membrane thickens
Makes hard to oxygen transfer
Hypoxia

Medium and large wall damage
Athersclerosis

192
Q

What systemic problems can diabetes cause?

A

Retinopathy

Kidneys
Nephrotic syndrome

Nerves
Decrease in sensation
Stocking-glove distribution

193
Q

WHAT IS CARCINOID SYNDROME?

What three symptoms are under the syndrome?

A

Specific type of tumour

Causes neuroendocrine cells to secrete hormones

Syndrome
Diarrhoea
SOB
Flushing

194
Q

Where are neuroendocrine cells found?

A

Epithelial layer of GI organs and lungs

195
Q

How are neuroendocrine cells activated and what can they release?

A

Nerves

Serotonin
Histamine

Bradykinin

Prostaglandins

196
Q

Where is somatostatin released from and what does it act on?

What does it inhibit?

A

Hypothalamus + GI tract

Acts on surface of neuroendocrine cells

Serotonin

197
Q

What happens to serotonin?

What is it metabolised to?

What happens to the reamining serotonin?

A

Goes to the liver through the portal vein where it is metabolised

5-hydroxyindoleacetic acid

Goes into blood stream

198
Q

What are the actions of serotonin?

A

GI
Increased motility and peristalsis

Blood vessels
Taken by platelets and constrict blood vessels

Heart
Stimulates fibroblasts to make collagen

199
Q

Where is the most common place for a cacinoid tumour and what do they also produce more of?

A

GI tract

Somatostatin receptors

200
Q

Where is the most common site for a neuroendocrine tumour to metastisize?

A

Liver

201
Q

What is often neccesary for carcinoid syndrome?

Why?

A

Metastatisis to the liver

Liver normally metabolises the hormones released from the tumours so they build up

Causing symptoms

202
Q

What does the increase in histamine and bradykinin do?

A

Dilates blood vessels causing flushing

203
Q

What does the increase in serotonin cause?

A

Fibrosis of heart
Tricuspid valve regugitation
Pulmonary stenosis

Bronchoconstriction
Asthma
Shortness of breath

**_Reduces tryptophan_**
Reduces niacin (vit b3)
Pellagra
204
Q

What are the symptoms of carcinoid syndrome?

A

Diarrhoea
SOB
Flushing
Itching

205
Q

What are symptoms of carcinoid syndrome worsened by?

A

Alcohol

Emotional stress

206
Q

What is the diagnosis for carcinoid syndrome?

A

CT scan

Octreoscan
Inject radioactive labelled octreotide
Binds to increase number of somatostatin

Urinalysis
5-hydroxyindoleacetic acid

Blood tests
Niacin deficiency

207
Q

What is the treatment for cacinoid syndrome?

A

Somatostatin analogues
Octreotide

Decrease
Emotional stress
Alcohol

Carcinoid tumour
Surgery
Chemo

208
Q

WHAT IS HYPOCALCEMIA?

A

Low calcium in the blood

<8.5mg/dl

209
Q

What detects a change in calcium?

A

Parathyroid cells called calcium sensing receptor

210
Q

What does parathyroid hormone do?

A

More

Increases release of calcium from bones

Kidneys to absorb more calcium

Kidneys to synthesie more calcitriol

Calcitriol makes the GI tract absorb more calcium

Keep extracellualr calcium in range
8.5-10mg/dl

211
Q

What happens if there is a high ph or alkolosis?

A

Very few protons around

COO- form of albumin

More negative

Calcium attracts more to albumin

Less free ionized calcium

Symptoms of hypocalcemia

212
Q

What are the causes for hypocalcaemia?

A

Vit D deficiency
Diet
Lack of sunlight
Malabsoption

Magnesium deficiency

Hypoparathyroidism

213
Q

What are the other sings and symptoms of low calcium?

A

Chvostek’s sign

Trousseau’s sign

Muscle cramps
Abdominal pain
Perioral tingling
Seizures

214
Q

How do you diagnose hypocalcemia?

A

Low calcium in blood <8.5mg/dl

ECG
Prolonged QT interval
Prolonged ST segments
Arrythmias

Lab tests
Parathyroid hormone
Vitamin D
Albumin
Phosporus
Magnesium

215
Q

What is the treatment of hypocalcemia?

A

Normalize calcium levels

Calcium gluconate

Vitamin D supplementation

216
Q

WHAT IS HYPERCALEMIA?

A

Higher than normal calcium levels in the blood >10.5mg/dl

217
Q

What happens when there is a low ph or acidosis?

A

Lots of protons

COO- pick up a proton

Become COOH

More COOH becomes more positive

Calcium and albumin repel eachother

Increase in ionized calcium in blood

218
Q

Whatare some causes of hypercalcemia?

A

Increased osteoclast activity
Increased parathyroid

Too much vitamin D
Diet or from supplements

Medications
Thiazide diuretics
Increased reabsorption

219
Q

What do the kidneys do when there is hypercalcemia?

A

Dump more calcium in urine

Hypercalciuria

Loss of fluid

Dehydration

Leads to calcium oxalte stones

220
Q

How is hypercalcemia diagnosed?

A

High levels of calcium in blood >10.5mg/dl

ECG
Bradycardia
AV block
Short QT interval
Osbourne wave

Lab tests
Parathyroid
Vitamin D
Albumin
Phosphorus
Magnesium

221
Q

What is the treatment of hypercalcemia?

A

HYDRATION

DIURETICS

GLUCOCORTICOIDS (EXCRETION)

BISPHOSPHONATES

222
Q

WHAT IS DIABETES INSIPIDUS?

A

Lack of ADH

223
Q

What happens from a lack of ADH?

A

Water not sufficiently reabsorbed from collecting duct

Large amounts of undiluteurine

224
Q

What are the symptoms of diabetes insipidus?

A

Polydipsia

Polyuria

Dehydration

Hypernatremia

225
Q

What is central and nephrotic diabetes insipidus?

A

Central problem with hypothamus and pituitary
ADH low

Nephrotic problem with kidneys
ADH high

226
Q

What are the causes of central diabetes insipidus?

A

Tumour

Lack of blood supply (incSheehan’s)

Impact/fracture

Surgical

Autoimmune

227
Q

What are the nephrogenic causes of diabetes insipidus?

A

Lithium toxicity

Release of obstruction

Hypercalcemia

Hypokalaemia

228
Q

How can you determine the cause of diabetes insipidus?

A

Give desmopressin

If urine output falls, osmolality increases

Suggests central

229
Q

What is the treatment of diabetes insipidus?

A

Central
Desomopressin

Diuretics
Hydrocholorothiazide

230
Q

Why do you give a patients diuretics with nephrotic diabetes insipidus?

A

Promote water AND SALT LOSS

Activate RAAS!!

231
Q

WHAT IS HYPERKALAEMIA?

A

High amount of potassium in the blood

> 5.5mmol/L

232
Q

What are the causes of hyperkalaemia?

A

External
Beta blocker
ACEi

Internal
Diabetes mellitus
Acidosis (H+ for K+ that are inside cells)
Rhabdomyolysis
Oliguric renal failure​
Addison’s
Burns

233
Q

What can hyperkalaemia lead to?

A

Myocardial excitability → VF and cardiac arrest

234
Q

How can you diagnose hyperkalaemia?

A

ECG

Tall tented T waves

Small P waves

Wide QRS (eventually becoming sinusoidal)

VF

235
Q

What is the treatment for hyperkalaemia?

A

Insulin
Drive K+ into cells

Treat underlying cause

Polystyrene sulfonate resin (binds K+ in gut)

Calcium gluconate (Stabilize membrane potential)

236
Q

WHAT IS HYPOKALAEMIA?

A

Low potassium in blood

< 3.5mmol/L

237
Q

What are the causes of hypokalaemia?

A

External
Diuretics; V/D

Internal
Excess Insulin
Alkolosis
Cushing’s
Conn’s (Increased aldosterone)

238
Q

What are the symptoms of hypokalaemia?

A

Smooth muscle
Constipation

Skeletal muscle
Weakness
Cramps

239
Q

How is hypokalaemia diagnosed?

A

Low potassium in blood

ECG
Prolonged QT interval
Prolonged PR interval
U wave
Arrthymias

240
Q

What is the treatment for hypokalaemia?

A

Treat underlying cause

Supplements

Potassium sparing diuretics

241
Q

WHAT DOES THE PARATHYROID DO?

What does this hormone do?

A

Release parathyroid hormone

Increases bone resorption

Increases calcium absorption in kidneys
Increases Vit D synthesis in kidney

Vit D increases GI absorption

242
Q

What does the thyroid release in high levels of calcium?

What does this do?

A

Calcitoin

Increase bone deposition

Decrease kidney absorption of calcium

243
Q

WHAT IS HYPERPARATHYROIDISM?

A

Increase in parathyroid hormone

244
Q

What are the different causes of hyperparathyroidism?

A

Primary
Adenoma

Secondary
PTH is high to attempt to correct persistently low calcium levels

Tertiary
After many years of uncorrected secondary hyperparathyroidism

245
Q

What are the symptoms of hyperparathyroidsm?

A

STONES, BONES and GROANS

Increased Ca2+
Weak, tired, depressed, thirsty, renal stones, abdopain.

Bone resorption
Pain, fractures, osteopenia/porosis.

Increased BP
Check Ca2+ in hypertension.

246
Q

What are the tests for primary hyperparathyroidism?

A

PTH
High

Calcium
High

Phosphate
Low

Phosphatase
High

247
Q

What is the treatment for primary hyperparathyroidism?

A

Treat underlying cause

248
Q

What are the causes of secondary hyperparathyroidism?

A

CKD

vit D deficiency

GI disease such as bypass and Crohn’sare also possible

249
Q

What are the symptoms for hyperparathyroidism?

A

Bony

Osteomalacia

250
Q

What are the tests for secondary hyperparathyroidism?

A

PTH
High

Calcium
Low

Phosphate
High

Phosphatase
High

251
Q

What is the treatment for secondary hyperparathyroidism?

A

Treat underlying cause

Bisphosphonates

252
Q

WHAT IS HYPOPARATHYROIDISM?

A

Low levels of parathyroid hormone

253
Q

What are the causes of hypoparathyroidism?

A

Primary
AI, congenital (Di George syndrome)

Secondary
Radiation, surgery, hypomagnesaemia

254
Q

What are the signs of hypoparathyroidism?

A

Hypocalcaemia

SPASMODIC

Spasms

Trousseau’s on inflation of cuff

anxious

seixures

Chvostek’s – tap facial nerve over parotid – corner of mouth twitches.

255
Q

What is the treatment of hypoparathyroidism?

A

Ca2+ supplements

Calcitriol (prevents hypercalciuria)

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