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ΩΩ 2a Bateman - Systems Based > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

WHAT IS ACROMEGALY?

What is it caused by?

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

A

This is an abnormal enlargement of the extremities of the skeleton caused by hypersecretion of the pituitary growth hormone after epiphysial fusion.

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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 is the difference between gigantism and acromegaly?

A

Difference in when growth hormone is released

gigantism - Before the closure of the epiphyseal plates, end up very tall

Acromegaly - After the closure of the epiphyseal plates

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4
Q

What is the cause of acromegaly?

A
  • 95% of cases are due to a growth hormone secreting pituitary adenoma
  • less than 3% of cases are due to ectopic GHRH production - carcinoid tumours especially bronchial, pancreatic islet tumours or adrenal tumours
  • less than 2% of cases result from ectopic GH secreting pancreatic islet tumours
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5
Q

What are the symptoms of acromegaly?

Go through each topic RS etc

A

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

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6
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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7
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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8
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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9
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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10
Q

WHAT IS CUSHING SYNDROME?

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

A

Cushing’s syndrome refers to the set of clinical features resulting from persistently and inappropriately elevated levels of glucocorticoid. Usually the condition is iatrogenic

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11
Q

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

A

Zona glomerulosa

Zona fasiculata

Zona reticularis

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12
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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13
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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14
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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15
Q

How is hypertension caused by excess cortisol?

A
  1. Amplifies effect of catecholamines on blood vessels
  2. Cortisol cross reacts with mineralcorticoid recptors
  3. Mineralcorticoids released from zona glomerulosa
  4. Triggers mineralcorticoid effect which is increasing blood pressure by retaining fluid - ALDOSTERONE
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16
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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17
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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18
Q

What is the diagnosis of Cushing’s?

A
  1. ENDOGENOUS / 24 urine sample
    – Measuring free cortisol - urine 3.5-4.5 microgram/day
    – 1 mg Dexamethasone suppresion test
    Low dose of dexamethasone (steroid)
    Supressess ACTH production
    Should cuase decrease cortisol levels <2
  2. 2mg Dexamethasone Supression Test
  3. ACTH plasma levels checked
    Low ACTH gives diagnosis of
    Adrenal adenomas and carcinoma

High ACTH gives diagnosis of
Cushing disease and ectopic ACTH production
4. 8mg Dexamethasone Supression
Pituitary - Cortisol + ACTH suppressed
Ectopic - Cortisol + ACTH NOT suppressed

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19
Q

What types of imaging can be used for Cushing’s?

A

MRI of pituitary

CT of adrenals

CT of chest abdomen or pelvis for ectopic

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20
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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21
Q

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

A

Nelson’s syndrome

Skin pigmentation increase

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22
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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23
Q

What causes SIADH?

A

Drug-induced

  • Selective serotonin reuptake inhibitors
  • Carbamazepine
  • Tricyclic antidepressants

Neoplastic

  • Small cell lung cancer
  • Mesothelioma
  • GI tract malignancy

Pulmonary

  • Pneumonia - especially Legionella and Mycoplasma
  • Tuberculosis

CNS

  • Tumour
  • Meningitis, encephalitis
  • Head injury

Miscellaneous

  • Guillain–Barre syndrome
  • Multiple sclerosis
  • Acute intermittent porphyria
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24
Q

What are the symptoms caused by in SIADH?

A

Derived from decreased sodium in the blood

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25
Q

What are the symptoms of SIADH?

A

Stupor/coma

Anorexia (nausea and vomiting)

Lethargy

Tendon reflexes decreased

Limp muscles (weakness)

Orthostatic hypotension

Seizures/headache

Stomach cramping

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26
Q

What is the diagnosis of SIADH?

A

Sodium

  • Plasma sodium concentration <135 mmol/l
  • Urinary sodium concentration >30mmol/L

Osmolality

  • Plasma osmolality <280 mOsmol/kg
  • Urine osmolality > 100 mOsmol/kg

Other

  • Patient clinically euvolaemic
  • Absence of clinical or biochemical features of adrenal and thyroid dysfunction.
  • No diuretic use (recent or past)
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27
Q

What is the treatment for SIADH?

A

Treat underlying cause

Acute

Hypertonic (3%) saline given via continuous infusion
Intravenous furosemide 20 to 40 mg

Chronic

For most other cases of mild-to-moderate SIADH, fluid restriction represents the least toxic therapy, and has generally been the treatment of choice

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28
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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29
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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30
Q

What are the causes of secondary hypothyroidism?

A

Hypopituitarism

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31
Q

What is the epidemology of hashimoto’s thyroiditis?

A

Older Women

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32
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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33
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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34
Q

What are the investigations for hypothyroidism?

A

TFT
TSH RAISED

Lipids/cholesterol
High

FBC
Macrocytosis

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35
Q

What are the disease 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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36
Q

What is the treatment of hypothyroidism?

A

Levothyroxine (T4)

Higher doses in the young

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37
Q

WHAT IS HASHIMOTO’s THYROIDITIS?

(inside hypothyroidism)

A

Autoimmune disease

T cell mediated attack

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38
Q

What are the symptoms of hasimoto’s thyroiditis?

A

Goitre or hypothyroidism or both

Enlargement is usually slow and painless but rarely, may be more rapid and painful

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39
Q

What are the investigations for hasmimoto’s thyroiditis?

A

The condition may be suspected clinically on the basis of the goitre with or without hypothyroidism.

  1. Serum TSH is usually raised
  2. Measurement of antithyroid antibodies reveal:
    * *- Thyroid peroxidase antibodies (TPO)** (previously known as thyroid microsomal antibodies) - TPO HIGH titre
    * *- Thyroglobulin antibodies (TgAb)** - HIGH titre
  3. Biopsy may be necessary to distinguish it from a carcinoma of the thyroid
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40
Q

What is the treatment of hasimoto’s thyroiditis?

A

If the patient is hypothyroid then oral thyroxine may keep the patient euthyroid and lead to resolution of the goitre.

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41
Q

WHAT IS HYPERTHYROIDISM?

A

Too much thyroid hormones

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42
Q

What are the causes of hyperthyroidism?

A
  1. GRAVES’ DISEASE
  2. TOXIC MULTINODULAR GOITRE
  3. EXOGENOUS (Iodine / T4 excess)
  4. DE QUERVAIN’S THYROIDITIS (post-viral)
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43
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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44
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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45
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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46
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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47
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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48
Q

What are the symptoms of graves disease?

A
  1. Hyperthyroidism
  2. Diffuse goitre
  3. Extrathyroid features:
    • Thyroid acropachy, a triad of:
      Digital clubbing
      Soft tissue swelling of the hands and feet
      Periosteal new bone formation
    • Graves’ ophthalmology - 40% of cases
    • Pretibial myxoedema - 5% of cases
    • Thyroid acropachy - rare
    • Onycholysis - not specific to Grave’s!!
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49
Q

What are the investigations for Grave’s disease?

A
  • Serum TSH
  • Free thyroxine (T4) & free or total triiodothyronine (T3
  • Serum levels of antibodies to the TSH receptor
  • Thyroid peroxidase and thyroglobulin autoantibodies
  • Radioactive iodine uptake and scan
  • Thyroid ultrasound scan
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50
Q

What is the treatment of Grave’s disease?

A
  1. Radioactive iodine - first-line
  2. Carbimazole
  3. Thyroidectomy
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51
Q

What are some causes of goitre?

A

Physiological

Graves’ disease

Hashimoto’s thyroiditis

De Quervain’s

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52
Q

WHAT ARE THE MOST LIKELY THYROID CELL TYPE CANCERS?

A

Papillary (60%)

Follicular (≤25%)

Medullary (5%)

Lymphoma (5%)

Anaplastic

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53
Q

What are some causes of thyroid cancer?

A

Low dose radiation

Radioiodine

A history of radiation exposure to the neck area is associated with increased risk of thyroid cancer

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54
Q

What are the symptoms of thyroid cancer?

A

A rapidly growing hard thyroid mass with lymphadenopathy and indicators of extrathyroidal invasion

e.g. hoarseness, dysphagia is suggestive of maligancy.

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55
Q

What are the investigations for thyroid cancer?

A

Fine needle biopsy - the most effective method of distinguishing benign from malignant nodules.

Tumour products - basal and pentagastrin-stimulated serum calcitonin distinguishes medullary carcinoma.

Ultrasound - not useful as a primary test but may help to distinguish cystic lesions

Thyroid scanning with radioiodine - thyroid cancer is characteristically

Chest X-ray - lung secondaries

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56
Q

What is the treatment for thyroid cancer?

A

Most thyroid tumours are treated surgically with follow up radioiodine ablation

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57
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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58
Q

What are the different layers of the adrenal glands?

A

Cortex
Zona glomerulosa
Zona fasiculata
Zona reticularis

Medulla

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59
Q

What does each layer of the adrenal cortex produce?

A
  1. Zona glomerulosa - Aldosterone
  2. Zona fasiculata - Cortisol and glucocorticoids
  3. Zona reticularis - Make androgens E.g. deyhydroepiandosterone, Precursor to testosterone
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60
Q

What does the renin, angiotensin aldosterone system do?

A

Decrease potassium

Increase sodium

Increase blood volume and pressure

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61
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

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62
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

63
Q

What are the symptoms if the zona glomerulosa is affected?

A

Cravings for salty foods

Nausea and vomiting

Fatigue

Dizzyness

64
Q

What are the symptoms 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

65
Q

What are the symptoms if the zona fasiculata is destroyed?

A

Fatigue in times of stress

Hyperpigmentation on knuckles and joints

66
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

67
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

68
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(↓)

69
Q

What is the treatment for addison’s disease?

A

Homones

Cortisol - hydrocortisone
Aldosterone - Fludrocortisone
Androgens

Take for life

Stopping can lead to crisis

70
Q

If a patient with Addison’s disease becomes acutely unwell what is needed to be done to their medications?

A
  1. Double the glucocorticoid
  2. Keep the fludrocortisone dose the same
71
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)

72
Q

What syndrome can cause an addisonian crisis?

A

Waterhouse-friderichsen syndrome

Causes blood vessels in adrenal glands to rupture

73
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

74
Q

WHAT IS SECONDARY ADRENAL INSUFFICIENCY?

A

Lack of ACTH

and therefore cortisol

75
Q

What are the causes for secondary adrenal insufficiency?

A

Medications
Glucocorticoids

Pituitary mass or infection

76
Q

Why is aldosterone unaffected in secondary adrenal insufficiency?

A

Aldosterone secretion independent of ACTH

77
Q

What are the symptoms of secondary adrenal insufficiency?

A

Features common to both primary and secondary hypoadrenalism include:

  1. Lassitude and muscle weakness and pain
  2. Hypotension
  3. Gastro-intestinal symptoms - anorexia, weight loss, nausea and vomiting, intermittent abdominal pain salt, craving
  4. Decrease in axillary and pubic hair - common in women
  5. Depression

Pigmentation only occurs in primary hypoadrenalism, due to high ACTH:

  1. The skin assumes a dull, grey-brown colouration
  2. Exposed skin, pressure areas, palmar creases, knuckles, buccal mucosa and recent scars are the commonest sites
78
Q

What is the diagnosis of secondary adrenal insufficiency?

A

Bloods
Low cortisol

79
Q

What is the treatment for secondary adrenal insufficiency?

A

Glucocorticoid analogues - hydrocortisone

10mg in morning, 5 mg at midday, 5mg in evening.

Fludrocortisone

80
Q

WHAT IS CONN’S SYNDROME?

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

A

Hyperaldosteronism

81
Q

What is the cause of Conn’s syndrome?

A

Adrenal adenima

Bilteral adrenal nodular hyperplasia

82
Q

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

A

Potassium low

Sodium high

Less protons

83
Q

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

A

Hypertension

Metabolic alkolosis

84
Q

What are the symptoms of Conn’s syndrome?

A

Headaches and flushing

Constipation
Weakness
Heart rhythm changes

85
Q

What is the diagnosis of Conn’s syndrome?

A

FIRST LINE ALDOSTERONE/RENIN RATIO - Bloods
High levels of aldosterone
Low levels of renin

Differentiate between adenoma and hyperplasia
CT

Hypokalaemia*- ensuring absence of diuretics, steroids, laxatives
​Hypernatraemia - sodium may be mildly elevated or normal
Hypertension
Metabolic alkalosis

86
Q

What is the treatment for Conn’s syndrome?

A

Potassium sparing diuretic
Spirinolactone

Surgery
Remove tumour

87
Q

WHAT DIABETES MELLITUS?

A

Trouble moving glucose from blood into cells

High level in blood

Not alot in cells

88
Q

What are the different types of diabetes?

A

Type 1
10%

Type 2
90%

89
Q

What is the cause of type 1 diabetes?

A

Bodies own cells attack the pancreas

Type 4 hypersensitivty reaction
Cell-mediated response

90
Q

What are the symptoms of type 1 diabetes?

A

Polydipsia

Polyuria, with associated nocturia or enuresis

Glycosuria

Weight loss due to dehydration and catabolism

Polyurea, polydipsia (due to osmotic diuresis), polyphagia,

Constipation

Fatigue

Cramps

Blurred vision

Bacterial and fungal infections e.g. - candidiasis

91
Q

What are some complications of diabetics with bad control?

A

Vascular disease

Nephropathy

Neuropathy

Diabetic foot

Retinopathy

92
Q

What are the investigations for type 1 diabetes?

A

Diabetes is diagnosed on the basis of history (ie polyuria, polydipsia and unexplained weight loss) PLUS

a random venous plasma glucose concentration >= 11.1 mmol/l

OR a fasting plasma glucose concentration >= 7.0 mmol/l (whole blood >= 6.1 mmol/l)

OR 2 hour plasma glucose concentration >= 11.1 mmol/l 2 hours after 75g anhydrous glucose in an oral glucose tolerance test (OGTT)

an HbA1c of 6.5% (48 mmol/mol) is recommended as the cut point for diagnosing diabetes (i.e. HbA1c >= 6.5% (48 mmol/mol) is sufficient for the diagnosis of diabetes)

93
Q

What is the treatment for type 1 diabetes?

A

Lifelong insulin injections

Education

94
Q

What is are the diabetic emergencies?

A

Hypoglycaemia

Hyperglycaemia

Diabetic ketoacidosis

Hyperosmolar non-ketotic hyperglycemia

95
Q

WHAT IS DIABETIC KETOACIDOSIS?

A

Biochemical triad of

  1. Ketonaemia
  2. Hyperglycaemia
  3. Acidaemia
96
Q

What can ketones do to the blood?

A

Make the blood acidic

Kussmaul respiration

Deep/labored breathing
To reduce CO2
Reduce acidity

97
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

98
Q

What are the symptoms of diabetic ketoacidosis?

A
  1. Polyuria with polydipsia – commonest presenting symptom
  2. Fatigue
  3. Dyspnea
  4. Vomiting
  5. Preceding febrile illness
  6. Abdominal pain
  7. Polyphagia
  8. Kussmaul respirations
  9. Acetone breath
99
Q

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

A

Acetone

Fruity smell

100
Q

What does ketoacidosis cause?

A

Nausea

Vomiting

Mental status changes

Cerebral oedema

101
Q

What are the investigations for DKA?

A
  1. Serum glucose level
    Usually greater than 250 mg/dL (13.9 mmol/L)
  2. Arterial blood gas measurement
    pH varies from 7.00 to 7.30
  3. Serum electrolytes
    Bicarbonate level - <18 mmol/L (18 mEq/L)
    Serum sodium level - usually low
    Serum potassium - may be low, normal, or elevated
    Magnesium – usually low but can be normal
  4. Blood urea nitrogen, creatinine levels
  5. Serum ketone level
  6. Urinalysis
    Confirms the presence of glucose and ketones
    Positive for leukocytes and nitrites in the presence of infection
102
Q

What is the diagnosis of DKA?

A
  1. Ketonaemia 3 mmol /l and over or significant ketonuria (more than 2 + on standard urine sticks)
  2. Blood glucose over 11 mmol /l or known diabetes mellitus
  3. Venous bicarbonate (HCO3 ) ) below 15 mmol /l and /or venous pH less than 7.3
103
Q

What is the treatment for diabetic ketoacidosis?

A

Fluids for dehydration - 0.9% sodium chloride

Insulin to lower blood glucose - 0.1 units/kg

Glucose when blood glucose falls below 14mmol/l

Electrolytes (K+)

104
Q

WHAT IS TYPE 2 DIABETES MELLITUS?

A

Body makes insulin but the cells don’t respond

Not fully understood

105
Q

What are the risk factors for type 2 diabetes?

A

Obesity

Lack of exercise

Hypertension

106
Q

What is normoglycemia?

A

Insulin levels high when cells don’t respond to insulin

Blood glucose levels remain normal

107
Q

What are the symptoms of type 2 diabetes mellitus?

A

polydipsia

polyuria, with associated nocturia or enuresis

glycosuria

108
Q

What is the test for diabetes type 2?

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

109
Q

What is the management of diabetes type 2?

A
  1. Metformin
  2. SU - e.g. Glipizide
  3. DPP-4i - GLIPTINS
  4. Pioglitazone
  5. SGLT-2i - GLIFLOZINS
110
Q

What systemic problems can diabetes cause?

A

Retinopathy

Kidneys
Nephrotic syndrome

Nerves
Decrease in sensation
Stocking-glove distribution

111
Q

How does metofrmin work?

A

Improves insulin sensitivity by

  1. Actions upon the liver:
    reducing hepatic gluconeogenesis and glycogen breakdown
  2. Actions upon skeletal muscle and adipose tissue:
    increasing insulin-stimulated glucose uptake and oxidation and, in muscle, increasing glycogen formation
112
Q

How do sulphoylureas work? SE?

A

Augmentation of secretion of insulin from pancreatic beta-cells.

Sulphonylureas may also cause a reduction in serum glucagon and potentiate the action of insulin at the extrapancreatic tissues

WEIGHT GAIN

113
Q

How do DDP-4i work?

A

In response to a meal, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) are released (these hormones are termed incretin hormones)

these incretin hormones stimulate insulin and suppress glucagon release (both in a glucose-dependent manner), delay gastric emptying, and increase satiety

incretins are rapidly degraded by dipeptidyl peptidase-4 (DPP-4)

DPP-4 inhibitors are a class of oral antihyperglycemic agents that work via slowing incretin degradation

DPP-4 inhibitors enhance meal-stimulated active GLP-1 and GIP levels by two- to threefold

114
Q

What is the difference between diabetes type 1 and diabetes type 2?

A

Factors favouring type 1

rapid onset of osmotic symptoms

normal or low body weight or rapid weight loss

ketonaemia >=3mmol/l on capillary testing or ketonuria

family or personal history of other autoimmnune conditions

failure to respond to oral therapy

positive antibody test (anti-GAD, insulin autoantibodies (IAA) and islet cell antibodies (ICA) most commonly used)

urine C-peptide:creatinine ratio less than 0.5nmol/l

115
Q

WHAT IS HYPERGLYCEMIC HYPEROSMOLAR STATE?

A

Extreme elevations in serum glucose concentrations, hyperosmolality and dehydration without significant ketosis

116
Q

What are the clinical features of HHS?

A

Hyperglycaemia

Dehydration with marked thirst

Marked drowsiness

Weakness

Visual disturbance

Leg cramps

Nausea and vomiting - less frequent than in patients with DKA

117
Q

What is the diagnostic criteria for HHS?

A

plasma glucose concentration >33.3 mmol/L (600 mg/dL)

arterial pH > 7.30; venous pH > 7.25

serum bicarbonate >15 mmol/L

small ketonuria, absent to small ketonemia

effective serum osmolality >320 mOsm/kg

obtundation, combativeness, or seizures (in approximately 50%)

118
Q

What is the management of HHS?

A

Fluids 0.9% sodium chloride

Insulin 0.1/kg
blood glucose insulin rate (u/hour)
>20 - 3

13-20 - 2

5-13 - 1

<5 - 0.5

If potassium low give them infusion

119
Q

WHAT IS CARCINOID SYNDROME?

What three symptoms are under the syndrome?

A

Specific type of tumour

Causes neuroendocrine cells to secrete hormones

  • *Syndrome**
  • *D**iarrhoea
  • *F**lushing
  • *S**OB
120
Q

Where are neuroendocrine cells found?

A

Epithelial layer of GI organs and lungs

Kulchitsky cells

Mid-gut

Hind-gut

121
Q

How are neuroendocrine cells activated and what can they release?

A

Nerves

  1. Serotonin
  2. Histamine
  3. Bradykinin
  4. Prostaglandins
122
Q

What are symptoms of carcinoid syndrome worsened by?

A
  1. Paroxysmal flushing - for example, following coffee, alcohol, certain foods and drugs
  2. Bronchoconstrictive episodes, similar to asthma
  3. Right-sided heart failure
  4. Episodes of explosive watery diarrhoea
  5. Abdominal pain
  6. Pellagra-like lesions of the skin and oral mucosa
123
Q

What are the investigations for carcinoid syndrome?

A

Urinalysis
5-hydroxyindoleacetic acid (5-HIAA)

Plasma Chromogranin A (CgA)

Octreoscan
Inject radioactive labelled octreotide
Binds to increase number of somatostatin

Blood tests
Niacin deficiency

124
Q

What is the treatment for cacinoid syndrome?

A

Somatostatin analogues
Octreotide

Decrease
Emotional stress
Alcohol

Carcinoid tumour
Surgery
Chemo

125
Q

WHAT IS DIABETES INSIPIDUS?

A

Lack of ADH

126
Q

What happens from a lack of ADH?

A

Water not sufficiently reabsorbed from collecting duct

Large amounts of undilute urine

127
Q

What are the symptoms of diabetes insipidus?

A
  1. Polydipsia
  2. Polyuria
  3. Dehydration
  4. Hypernatremia
128
Q

What is central and nephrotic diabetes insipidus?

A

Central problem with hypothamus and pituitary
ADH low

Nephrotic problem with kidneys
ADH high

129
Q

What are the causes of central diabetes insipidus?

A
  1. Tumour
  2. Lack of blood supply (inc Sheehan’s)
  3. Impact/fracture
  4. Surgical
  5. Autoimmune
130
Q

What are the nephrogenic causes of diabetes insipidus?

A
  1. Lithium toxicity
  2. Release of obstruction
  3. Hypercalcemia
  4. Hypokalaemia
131
Q

How can you determine the cause of diabetes insipidus?

A

Give desmopressin

If urine output falls, osmolality increases

Suggests central

132
Q

What is the treatment of diabetes insipidus?

A

Central
Desomopressin 5-40mg intranasally

Diuretics
Hydrocholorothiazide

133
Q

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

A

Promote water AND SALT LOSS

Activate RAAS!!

134
Q

WHAT IS THE DIFFERENCE BETWEEN DIABETES INSIPIDUS VS SIADH?

135
Q

WHAT DOES THE PARATHYROID DO?

What does this hormone do?

A

Release parathyroid hormone

  1. Increases bone resorption
  2. Increases calcium absorption in kidneys
  3. Increases Vit D synthesis in kidney
    • Vit D increases GI absorption
136
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

137
Q

WHAT IS HYPERPARATHYROIDISM?

A

Increase in parathyroid hormone

138
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

139
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.

140
Q

What are the tests for primary hyperparathyroidism?

A

PTH
High

Calcium
High

Phosphate
Low

Phosphatase
High

141
Q

What is the treatment for primary hyperparathyroidism?

A

Treat underlying cause

142
Q

What are the causes of secondary hyperparathyroidism?

A

CKD

vit D deficiency

GI disease such as bypass and Crohn’sare also possible

143
Q

What are the symptoms for hyperparathyroidism?

A

Bony

Osteomalacia

144
Q

What are the tests for secondary hyperparathyroidism?

A

PTH
High

Calcium
Low

Phosphate
High

Phosphatase
High

145
Q

What is the treatment for secondary hyperparathyroidism?

A

Treat underlying cause

Bisphosphonates

146
Q

WHAT IS HYPOPARATHYROIDISM?

A

Low levels of parathyroid hormone

147
Q

What are the causes of hypoparathyroidism?

A

Primary
AI, congenital (Di George syndrome)

Secondary
Radiation, surgery, hypomagnesaemia

148
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.

149
Q

What is the treatment of hypoparathyroidism?

A

Ca2+ supplements

Calcitriol (prevents hypercalciuria)

150
Q

WHAT IS PHAEOCHROMOCYTOMA?

A

Catecholamine secreting tumour

151
Q

What are the clinical features of phaeochromocytoma?

A

hypertension (around 90% of cases, may be sustained)

headaches

palpitations

sweating

anxiety

152
Q

What are the investigations for phaeochromocytoma?

A

24 hr urinary collection of metanephrines

replaced 24hr collection of catecholamines

153
Q

What is the management for phaeochromocytoma?

A
  1. Surgery is definitive
  2. Alpha-blocker (e.g. phenoxybenzamine) before
  3. Beta-blocker (e.g. propranolol)

ΩΩ 2a Bateman - Systems Based (11 decks)

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