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ΩΩ 4 Bateman - Specialities + Endo + GI + Liver > Endocrinology > Flashcards

Endocrinology Flashcards

(210 cards)

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1
Q

What peptide is used in making insulin?

A

C-peptide

Gliclazide functions by releasing vesicles stored within the pancreas containing insulin and C-peptide. This happens because insulin is derived from proinsulin and C-peptide is formed as a byproduct.

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2
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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3
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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4
Q

What is the difference between gigantism and acromegaly?

A

Difference in when growth hormone is released

  1. Gigantism - Before the closure of the epiphyseal plates, end up very tall
  2. Acromegaly - After the closure of the epiphyseal plates
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5
Q

What is the cause of acromegaly?

A
  1. 95% of cases are due to a growth hormone secreting Pituitary adenoma
  2. Less than 3% of cases are due to ectopic GHRH production - carcinoid tumours especially bronchial, pancreatic islet tumours or adrenal tumours
  3. Less than 2% of cases result from ectopic GH secreting pancreatic islet tumours
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6
Q

What are the symptoms of acromegaly?

A
  1. Coarse facial appearance, spade-like hands, increase in shoe size
  2. Large tongue, prognathism, interdental spaces
  3. Excessive sweating and oily skin: caused by sweat gland hypertrophy
  4. Features of pituitary tumour: hypopituitarism, headaches, bitemporal hemianopia
  5. Raised prolactin in 1/3 of cases → galactorrhoea
  6. 6% of patients have MEN-1
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7
Q

What are the signs of acromegaly?

A
  1. Skin darkening
    • Acanthosis nigricans
    • Face
  2. Big supraorbital ridge
    • Interdental separation
    • Macroglossia
    • Prognathism
    • Laryngeal dyspnoea
  3. Spade-like hands and feet
    • Tight rings
    • Carpal tunnel syndrome
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8
Q

How can you diagnose acromegaly?

A
  1. IGF-1 (somatomedin) tells tissues to grow
    • Elevated
  2. Glucose tolerance test
    • 75g or glucose
    • Wait 90 mins measure growth hormone levels
    • Will stay elevated! Should decrease
  3. Pituitary MRI
    • Could be no tumour, could be ectopic source

Growth hormone levels
Not usually used because pulsatile

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9
Q

What is the treatment of acromegaly?

A
  1. Trans-sphenoidal Surgery - FIRST LINE
  2. Medications to suppress GH
    • ​​Somatostatin analogue
      • Octreotide
    • Recombinant GH receptor antagonist
      • Pegvisomant
    • Dopamine agonist
      • Bromocriptine
  3. Radiation is sometimes used in older patinets or failed medicaitons
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10
Q

What are the complications of acromegaly?

A
  1. Hypertension
  2. Diabetes (>10%)
  3. Cardiomyopathy - MAIN CAUSE OF DEATH
  4. Colorectal cancer
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11
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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12
Q

What is the electrolyte abnormality in cushing syndrome?

A

Hypokalaemic metabolic alkalosis

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13
Q

What does excess cortisol lead to?

Overload of what it normally reacts with

A
  1. Severe muscle, bone and skin breakdown
  2. Hypertension
  3. Inhibit gonadotropin releasing hormone from hypothalamus
  4. Dampens inflammatory response
  5. More susceptible to infections
  6. Impair normal brain function
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14
Q

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

(What does this produce)

IN CUSHINGS

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
  1. ACTH dependent causes
    • Cushing’s disease (80%): pituitary tumour secreting ACTH producing adrenal hyperplasia
    • Ectopic ACTH production (5-10%): e.g. small cell lung cancer is the most common causes
  2. ACTH independent causes
    • Iatrogenic: steroids
    • adrenal adenoma (5-10%)
    • adrenal carcinoma (rare)
    • Carney complex: syndrome including cardiac myxoma
    • micronodular adrenal dysplasia (very rare)
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17
Q

What are the symptoms of Cushing’s?

A
  1. Muscle wasting and thin extemities
  2. Easy brusing
  3. Abdominal striae
  4. Fractues - osteoporisis
  5. Full moon shaped face
  6. Buffalo hump
  7. Truncal obesity
  8. Hypergylcemia
  9. Diabetes mellitius
  10. Hypertension
  11. Cardiovascular disease risk
  12. Increase vulnerability to infections
  13. Poor wound healing
  14. Amenorrhea
  15. 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
  2. 1 mg Dexamethasone suppresion test
    • Low dose of dexamethasone (steroid)
    • Supressess ACTH production
    • Should cuase decrease cortisol levels <2
  3. 2mg Dexamethasone Supression Test
    • ACTH plasma levels checked
      • Low ACTH + Cotrisol gives diagnosis of
      • Adrenal adenomas and carcinoma
      • High ACTH + Cortisol 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
  1. MRI of pituitary
  2. CT of adrenals
  3. CT of chest abdomen or pelvis for ectopic
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20
Q

What is the treatment for Cushing’s?

A
  1. Exogenous
    • Drug is gradually stopped
    • Adrenal crisis if too fast
    • Adrenal glands might be atrophied
  2. Endogenous
    • Surgery
    • Adrenal steroid inhibitors - Ketoconazole and metyrapone
    • Most useful ectopic

ALL PATIENTS MUST UNDERGO LABROATORY EVALUATIONS SCREENING FOR HORMONE HYPERSECRETION AND HYPOPITUITARISM

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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
  1. Hyponatremia and hypo-osmolality
  2. From inappropriate, continued secretion of ADH
  3. Despite normal or increased plasma volume
  4. 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
What are the symptoms of SIADH?
Stupor/coma Anorexia (nausea and vomiting) Lethargy Tendon reflexes decreased Limp muscles (weakness) Orthostatic hypotension Seizures/headache Stomach cramping
26
What is the diagnosis of SIADH?
**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)
27
What is the treatment for SIADH?
**_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
28
WHAT IS PRIMARY AND SECONDARY HYPOTHYROIDISM?
Primary is a reduction in thyroxin (T4) Secondary is a reduction in TSH
29
What are the causes of primary hypothyroidism?
1. Primary atrophic hypothyroidism (No goitre) 2. Hashimoto’s thyroiditis (Goitre) 3. Iodine deficiency 4. Post-thyroidectomy / radioiodine / antithyroid drugs 5. Lithium / amiodarone
30
What are the causes of secondary hypothyroidism?
Hypopituitarism
31
What is the epidemology of hashimoto's thyroiditis?
Older Women
32
What are the symptoms of hypothyroidism?
**_RS_** Hoarse voice **_GI_** Constipation **_Int_** Cold intolerance **_Endo_** Weight gain **_UG_** Menorrhagia **_MSK_** Myalgia, weakness **_Neuro / Psych_** Tired, low mood, dementia
33
What are the signs of hypothyroidism?
* *_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
34
What are the investigations for hypothyroidism?
1. **TFT** * TSH RAISED 2. **Lipids/cholesterol** * High 3. **FBC** * Macrocytic anaemia
35
What are the disease associations of hypothyroidism?
**AUTOIMMUNE** 1. VITILIGO 2. Type 1 Diabetes Mellitus 3. Addison’s disease 4. Pernicious anaemia 5. Primary biliary cirrhosis **INHERITED** 1. Turner’s syndrome 2. Down’s syndrome 3. Cystic fibrosis
36
What is the treatment of hypothyroidism?
1. Levothyroxine (T4) 2. Higher doses in the young
37
When should calcium be taken if patient is also taking levothyroxine?
Calcium 4 hours after levothyroxine
38
WHAT A HYPOTHYROID CRISIS?
Myxoedemic coma
39
What are the features of myxoedema coma?
Myxoedema coma typically presents with confusion and hypothermia
40
What is the treatment of a myxoedema coma?
1. **IV thyroid replacement** 2. **IV corticosteroids (until the possibility of coexisting adrenal insufficiency has been excluded)** 3. THEN IV fluid 4. electrolyte imbalance correction 5. sometimes rewarming
41
WHAT IS HASHIMOTO's THYROIDITIS? | (inside hypothyroidism)
Autoimmune disease T cell mediated attack
42
What are the symptoms of hasimoto's thyroiditis?
1. Goitre or hypothyroidism or both 2. Enlargement is usually slow and painless but rarely, may be more rapid and painful
43
What are the investigations for hasmimoto's thyroiditis?
The condition may be suspected clinically on the basis of the goitre with or without hypothyroidism. 1. **Serum TSH** is usually raised * Measurement of antithyroid antibodies reveal: * *Thyroid peroxidase antibodies (TPO)** (previously known as thyroid microsomal antibodies) - **HIGH titre** * **Thyroglobulin antibodies (TgAb)** - **HIGH titre** 2. **Biopsy** may be necessary to distinguish it from a carcinoma of the thyroid
44
What is the treatment of hasimoto's thyroiditis?
1. If the patient is hypothyroid then oral thyroxine may keep the patient euthyroid and lead to resolution of the goitre.
45
WHAT IS TOXIC MULTINODULAR GOITRE?
Toxic multinodular goitre describes a thyroid gland that contains a number of autonomously functioning thyroid nodules resulting in hyperthyroidism
46
What is the treatment for toxic multinodular goitre?
1. Radioactive iodine
47
WHAT IS HYPERTHYROIDISM?
Too much thyroid hormones
48
What are the causes of hyperthyroidism?
1. GRAVES’ DISEASE 2. TOXIC MULTINODULAR GOITRE 3. EXOGENOUS (Iodine / T4 excess) 4. DE QUERVAIN’S THYROIDITIS (post-viral)
49
What are the symptoms of hyperthyroidism?
**_CVS_** Palpitations **_GI_** Diarrhoea **_Int_** Heat intolerance **_Endo_** ↓Weight, ↑appetite **_UG_** Oligomenorrhoea +/- infertility **_Neuro / Psych_** Tremor, irritability, labile emotions
50
What are the signs of hyperthyroidism?
**_HANDS_** Palmar erythema; warm, moist skin; fine tremor **_PULSE_** Tachycardia; SVT; AF **_FACE_** Thin hair; lid lag / retraction **_NECK_** Goitre; nodules; bruit
51
What are the investigations for hyperthyroidism?
1. **TFT** * Increase T4 and T4 2. **FBC** * Normocytic anaemia 3. **ESR (↑)** 4. **Calcium (↑)** 5. **LFT (↑)** 6. **Thyroid autoantibodies** 7. **Visual fields, acuity, eye movements**
52
What is the treatment for hyperthyroidism?
Depends on underlying cause 1. **β-blockers** * Propanolol(rapid control of symptoms) 2. **Antithyroid medication** * Carbimazole SE = AGRANULOCYTOSIS * Block and replace (carbimazole + thyroxine) * Propythiouracil 3. **Radioiodine (131I)** 4. Thyroidectomy
53
WHAT HAPPENS IN GRAVES DISEASE? What are the triggers?
Autoimmune IgG autoantibodies bind to and stimulate TSH receptors Infection, stress, childbirth
54
What is a risk factor for grave's?
Smoking
55
What are the symptoms of graves disease?
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!!
56
What are the investigations for Grave's disease?
1. **Thyroid peroxidase antibodies** 2. **TSH receptor stimulating antibodies** 3. Radioactive iodine uptake and scan * Diffuse, homogenous, increase uptake of radioactive idodine 4. Thyroid ultrasound scan
57
What is the treatment of Grave's disease?
1. Propanolol * Use to help block the adrengergic effects 2. Carbimazole - first-line 3. Radioactive idodine 4. Thyroidectomy
58
What are some causes of goitre?
1. Physiological 2. Graves’ disease 3. Hashimoto’s thyroiditis 4. De Quervain’s - TENDER GOITRE
59
WHAT IS A THYROID STORM?
Thyroid storm is a rare but life-threatening complication of thyrotoxicosis. It is typically seen in patients with established thyrotoxicosis and is rarely seen as the presenting feature. Iatrogenic thyroxine excess does not usually result in thyroid storm.
60
What are the precipitating events to a thyroid storm?
1. thyroid or non-thyroidal surgery 2. trauma 3. infection 4. acute iodine load e.g. CT contrast media
61
What are the clinical features of a thyroid storm?
1. fever \> 38.5ºC 2. tachycardia 3. confusion and agitation 4. nausea and vomiting 5. hypertension 6. heart failure 7. abnormal liver function test - jaundice may be seen clinically
62
What is the management of a thyroid storm?
1. Symptomatic treatment e.g. paracetamol 2. Treatment of underlying precipitating event 3. **Beta-blockers: typically IV propranolol** 4. **Anti-thyroid drugs: e.g. methimazole or propylthiouracil** 5. Lugol's iodine 6. Dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3
63
WHAT ARE THE MOST LIKELY THYROID CELL TYPE CANCERS?
1. Papillary (60%) 2. Follicular (≤25%) 3. Medullary (5%) 4. Lymphoma (5%) 5. Anaplastic
64
What are some causes of thyroid cancer?
1. Low dose radiation 2. Radioiodine 3. A history of radiation exposure to the neck area is associated with increased risk of thyroid cancer
65
What are the symptoms of thyroid cancer?
A rapidly growing hard thyroid mass with lymphadenopathy and indicators of extrathyroidal invasion e.g. hoarseness, dysphagia is suggestive of maligancy.
66
What are the investigations for thyroid cancer?
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
67
What is the treatment for thyroid cancer?
Most thyroid tumours are treated surgically with follow up radioiodine ablation
68
What is used to yearly to detect for early thyroid cancer reoccurance?
1. Thyroglobulin levels 2. Except in medullary - calcitonin
69
WHAT IS PRIMARY ADRENAL INSUFFIENCY? https://www.youtube.com/watch?v=V6XcBp8EV7Q
The adrenal glands can't produce enough hormones Aldosterone and cortisol Primary refers to the adrenal glands themselves
70
What are the different layers of the adrenal glands?
**_Cortex_** Zona glomerulosa Zona fasiculata Zona reticularis **_Medulla_**
71
What does each layer of the adrenal cortex produce?
1. Zona glomerulosa - Aldosterone 2. Zona fasiculata - Cortisol and glucocorticoids 3. Zona reticularis - Make androgens E.g. deyhydroepiandosterone, Precursor to testosterone
72
What does the renin, angiotensin aldosterone system do?
Decrease potassium Increase sodium Increase blood volume and pressure
73
What are the causes of primary adrenal insuffiency?
1. **Autoimmune destruction** 2. Tuberculosis 3. Metastases (e.g. bronchial carcinoma) 4. Meningococcal septicaemia (Waterhouse-Friderichsen syndrome) 5. HIV 6. Antiphospholipid syndrom
74
What happens if the zona glomerulosa is destroyed?
1. Aldosterone levels fall 2. Leads to high potassium levels in the blood 3. Low sodium - hyponatremia 4. Low sodium water moves out of the blood vessels 5. Hypovolemia 6. High protons in blood 7. Metabolic acidosis since it's caused by the kidneys
75
What are the symptoms if the zona glomerulosa is affected?
Cravings for salty foods Nausea and vomiting Fatigue Dizzyness
76
What are the symptoms if the zona fasiculata is destroyed?
Fatigue in times of stress Hyperpigmentation on knuckles and joints
77
What happens if the zona reticularis is destroyed?
Men not affected Testes major source of male androgens Females Loss of pubic hair decreased sex drive
78
What does primary adrenal insuffiency usually need to cause symptoms?
Symptoms often slow, Major stressor comes along Injury, surgery or infection Cause symptoms to appear Sudden need for aldosterone and cortisol
79
How can you diagnose addison's disease?
1. **ACTH hormone test** * Small amount of synthetic ACTH injected * Measure cortisol and aldosterone produced * Both will be low 2. **Serum cortisol** 3. **Bloods** * FBC(anaemia, eosinophilia) * U&E(↓Na+, ↑K+, ↑Ca2+, ↑Urea) * BM(↓)
80
What is the treatment for addison's disease?
1. Cortisol - hydrocortisone 2. Aldosterone - Fludrocortisone 3. Dehydroepiandrosterone (DHEA)
81
If a patient with Addison's disease becomes acutely unwell what is needed to be done to their medications?
1. Double the glucocorticoid 2. Keep the fludrocortisone dose the same
82
What is it called when the body suddenly needs aldosterone or cortisol and the body can't deliver?
Addisonian crisis (acute primary adrenal insufficiency)
83
What syndrome can cause an addisonian crisis?
Waterhouse-friderichsen syndrome Causes blood vessels in adrenal glands to rupture
84
What are the symptoms of addisonian crisis?
1. Pain in back abdomen or legs 2. Vomiting and diarrhoea leading to dehydration 3. Low blood pressure leading to loss of consciousness 4. Death
85
What is the treatment of an Addisonian crisis?
1. **Hydrocortisone 100 mg im or iv** 2. 1 litre normal saline infused over 30-60 mins or with dextrose if hypoglycaemic 3. Continue hydrocortisone 6 hourly until the patient is stable. No fludrocortisone is required because high cortisol exerts weak mineralocorticoid action 4. Oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days
86
WHAT IS SECONDARY ADRENAL INSUFFICIENCY?
Lack of ACTH and therefore cortisol
87
What are the causes for secondary adrenal insufficiency?
1. Pituitary mass or infection * The basic failure is in the elaboration of ACTH
88
Why is aldosterone unaffected in secondary adrenal insufficiency?
Aldosterone secretion independent of ACTH
89
What are the symptoms of secondary adrenal insufficiency?
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
90
What is the diagnosis of secondary adrenal insufficiency?
**_Bloods_** Low cortisol
91
What is the treatment for secondary adrenal insufficiency?
1. **Glucocorticoid analogues - hydrocortisone** * 10mg in morning * 5 mg at midday * 5mg in evening 2. **Fludrocortisone** * ​​One dose ## Footnote **​​**
92
What is the cause of tertiary adrenal insufficiency?
Chronic administration of high doses of glucocorticoids
93
WHAT IS CONN'S SYNDROME? https://www.youtube.com/watch?v=JBfkGNr01V8&t=1s
Hyperaldosteronism
94
What is the cause of Conn's syndrome?
1. Bilteral adrenal nodular hyperplasia - MOST COMMON 2. Adrenal adenoma
95
If there is high aldosterone levels, what will the ion levels be in the blood?
Potassium low Sodium high Less protons
96
What do the ions in the blood in conn's syndrome cause?
Hypertension Metabolic alkolosis
97
What are the symptoms of Conn's syndrome?
Headaches and flushing Constipation Weakness Heart rhythm changes
98
What is the diagnosis of Conn's syndrome?
**Preliminary investigations** 1. **Hypokalaemia**\*- ensuring absence of diuretics, steroids, laxatives 2. **​Hypernatraemia** - sodium may be mildly elevated or normal 3. **Hypertension** 4. **Metabolic alkalosis** **Special investigations** 1. **Bloods - aldosterone/renin ratio** * High levels of aldosterone * Low levels of renin 2. 24 hour urinary aldosterone - raised in primary disease **Differentiate between adenoma and hyperplasia** 1. CT 2. **Adrenal vein sampling** 3. Measure plasma aldosterone 9am after overnight recumbency
99
What is the treatment for Conn's syndrome?
1. Identification of underlying cause 2. If due to **adenoma** * Surgery after 4 to 6 weeks of spironolactone therapy 3. if due to **adrenal hyperplasia** * Spironolactone or amiloride is generally sufficient
100
WHAT DIABETES MELLITUS?
Trouble moving glucose from blood into cells High level in blood Not alot in cells
101
What are the different types of diabetes?
Type 1 10% Type 2 90%
102
What is the cause of type 1 diabetes?
Bodies own cells attack the pancreas Type 4 hypersensitivty reaction Cell-mediated response
103
What are the symptoms of type 1 diabetes?
1. Polydipsia 2. Polyuria, with associated nocturia or enuresis 3. Glycosuria 4. Weight loss due to dehydration and catabolism 5. Polyurea, polydipsia (due to osmotic diuresis), polyphagia, 6. Constipation 7. Fatigue 8. Cramps 9. Blurred vision 10. Bacterial and fungal infections e.g. - candidiasis
104
What are some complications of diabetics with bad control?
Vascular disease Nephropathy Neuropathy Diabetic foot Retinopathy
105
What are the investigations for type 1 diabetes?
Diabetes is diagnosed on the basis of history (ie polyuria, polydipsia and unexplained weight loss) PLUS 1. A random venous plasma glucose concentration \>= 11.1 mmol/l 2. OR a fasting plasma glucose concentration \>= 7.0 mmol/l (whole blood \>= 6.1 mmol/l) 3. OR 2 hour plasma glucose concentration \>= 11.1 mmol/l 2 hours after 75g anhydrous glucose in an oral glucose tolerance test (OGTT) 4. 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)
106
What is the treatment for type 1 diabetes?
Lifelong insulin injections Education
107
What are the diabetic emergencies?
1. Hypoglycaemia 2. Hyperglycaemia 3. Diabetic ketoacidosis 4. Hyperosmolar non-ketotic hyperglycemia
108
What are the sick day rules for diabetes mellitus?
1. Increase frequency of blood glucose monitoring to **four hourly or more frequently** 2. Encourage **fluid intake** aiming for at least 3 litres in 24hrs 3. If unable to take struggling to eat may need sugary drinks to maintain carbohydrate intake 4. It is useful to educate patients so that they have a box of 'sick day supplies' that they can access if they become unwell 5. Access to a mobile phone has been shown to reduce progression of ketosis to diabetic ketoacidosis
109
What is it important not to stop when a diabetic patient is sick?
Their normal medication Keep taking insulin
110
What is the first line antihypertensive for a diabetes type 2 patient?
1. ACE inhibitor 2. ARB if black african
111
When do diabetic patients need to inform the DVLA and surrender their license?
After more than one hypoglycaemic episode requiring help
112
How often should diabetic patients measure their blood glucose?
At least 4 times a day, including before each meal and before bed
113
Which condition is important to factor in when measuring HbA1c in diabetic patients?
Hereditary spherocytosis Sickle cell Anytnhing that makes red blood cells live longer
114
What is the treatment of a peripheral neuropathy e.g. diabetic?
1. First-line treatment: **amitriptyline, duloxetine, gabapentin or pregabalin** 2. If the first-line drug treatment does not work try one of the other 3 drugs 3. **Tramadol** may be used as 'rescue therapy' for exacerbations of neuropathic pain 4. Topical capsaicin may be used for localised neuropathic pain (e.g. post-herpetic neuralgia) 5. Pain management clinics may be useful in patients with resistant problems
115
What are the rules for driving a HGV with diabetes?
1. Can drive a HGV 2. Must meet hypoglycaemic control standards
116
WHAT IS DIABETIC KETOACIDOSIS?
Biochemical triad of 1. Ketonaemia 2. Hyperglycaemia 3. Acidaemia
117
What can ketones do to the blood?
Make the blood acidic Kussmaul respiration Deep/labored breathing To reduce CO2 Reduce acidity
118
How can a diabetic ketoacidosis happen in somebody who already has insulin treatment?
1. A stress e.g. infection 2. Release of epinephrine 3. Release of glucagon 4. More glucose in blood 5. Loss of glucose in urine 6. Loss of water 7. Dehydration Need for alternative energy Generation of ketone bodies
119
What are the symptoms of diabetic ketoacidosis?
1. **Polyuria with polydipsia** – commonest presenting symptom 2. Vomiting 3. Preceding febrile illness 4. Abdominal pain 5. **Kussmaul respirations** 6. **Acetone breath**
120
What do the ketone bodies break down into? What does this cause to the breath?
Acetone Fruity smell
121
What are the investigations for DKA?
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
122
What is the diagnostic criteria of DKA?
1. Glucose \> 11 mmol/l or known diabetes mellitus 2. pH \< 7.3 3. Bicarbonate \< 15 mmol/l 4. Ketones \> 3 mmol/l or urine ketones ++ on dipstick
123
What is the treatment for diabetic ketoacidosis?
1. **Fluids for dehydration** * 0.9% sodium chloride 2. **Insulin to lower blood glucose** * 0.1 units/kg/hour 3. **When blood glucose falls below 15 mmol/l** * 5% dextrose 4. **Electrolytes (K+)** 5. **Long-acting insulin continued should be continued, short-acting insulin should be stopped**
124
What is definied as DKA resolution?
1. pH \>7.3 and 2. Blood ketones \< 0.6 mmol/L and 3. Bicarbonate \> 15.0mmol/L
125
What are the complication of DKA?
1. Gastric stasis 2. Thromboembolism 3. Arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia 4. Iatrogenic due to incorrect fluid therapy: cerebral oedema\*, hypokalaemia, hypoglycaemia 5. Acute respiratory distress syndrome 6. Acute kidney injury
126
What is the difference between diabetic and alcoholic ketoacidosis?
1. Normal or low glucose in alcoholic ketoacidosis
127
What is the first-line treatment for newly diagnosed diabetic patients after a DKA?
Basal-bolus insulin regimen with twice-daily insulin detemir
128
WHAT IS TYPE 2 DIABETES MELLITUS?
Body makes insulin but the cells don't respond Not fully understood
129
What are the risk factors for type 2 diabetes?
Obesity Lack of exercise Hypertension
130
What is normoglycemia?
Insulin levels high when cells don't respond to insulin Blood glucose levels remain normal
131
What are the symptoms of type 2 diabetes mellitus?
1. Polydipsia 2. Polyuria, with associated nocturia or enuresis 3. Glycosuria
132
What is the test for diabetes type 2?
**_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
133
What are the investigations for diabetic nephropathy?
1. all patients should be screened annually using urinary albumin:creatinine ratio (ACR) 2. should be an early morning specimen 3. ACR \> 2.5 = microalbuminuria Start with a spot urine sample If abnormal then do first-pass morning urine specimin
134
What do asymptomatic diabetic patients with a high HbA1c need?
Another HbA1c to confirm
135
What is the management of diabetes type 2?
1. **Metformin** 2. **SU - e.g. Gliclazide - HYPOHLYCAEMIA - HNF-1 alpha** 3. **DPP-4i - GLIPTINS** 4. Pioglitazone 5. SGLT-2i - GLIFLOZINS - Genitalia (fournier's gangrene)
136
What systemic problems can diabetes cause?
Retinopathy Kidneys Nephrotic syndrome Nerves Decrease in sensation Stocking-glove distribution
137
How does metformin work?
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
138
How do sulphoylureas work? SE?
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
139
How do DDP-4i work?
1. 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) 2. These **incretin hormones** stimulate **insulin** and **suppress glucagon** release (both in a glucose-dependent manner), delay gastric emptying, and increase satiety 3. **Incretins** are rapidly degraded by **dipeptidyl peptidase-4 (DPP-4)** 4. DPP-4 inhibitors are a class of oral antihyperglycemic agents that work via **slowing incretin degradation** 5. DPP-4 inhibitors enhance **meal-stimulated active GLP-1** and **GIP levels** by two- to threefold
140
What is the difference between diabetes type 1 and diabetes type 2?
Factors favouring type 1 1. Rapid onset of osmotic symptoms 2. Normal or low body weight or rapid weight loss 3. Ketonaemia \>=3mmol/l on capillary testing or ketonuria 4. Family or personal history of other autoimmnune conditions 5. Failure to respond to oral therapy 6. Positive antibody test (anti-GAD, insulin autoantibodies (IAA) and islet cell antibodies (ICA) most commonly used) 7. Urine C-peptide:creatinine ratio less than 0.5nmol/l
141
What is needed for impaired fasting glucose?
Two readings 6.1-7 mmol/l
142
WHAT IS HYPERGLYCEMIC HYPEROSMOLAR STATE?
Extreme elevations in serum glucose concentrations, hyperosmolality and dehydration **without** significant ketosis
143
What are the clinical features of HHS?
1. **General** * **​​**Fatigue, lethargy, nausea and vomiting 2. **Neurological** * Altered level of consciousness, headaches, papilloedema, weakness 3. **Haematological** * Hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis) 4. **Cardiovascular** * Dehydration, hypotension, tachycardia
144
What is the diagnostic criteria for HHS?
1. **Hypovolaemia** 2. Marked **Hyperglycaemia** (\>30 mmol/L) without significant ketonaemia or acidosis 3. Significantly raised **serum osmolarity** (\> 320 mosmol/kg) Also useful is: 1. Arterial pH 2. Serum bicarbonate \>15 mmol/L 3. Small ketonuria, absent to small ketonemia 4. Obtundation, combativeness, or seizures (in approximately 50%)
145
What is the management of HHS?
The goals of management of HHS can be summarised as follows: 1. Normalise the osmolality (gradually) * the serum osmolality is the key parameter to monitor * if not available it can be estimated by 2 \* Na+ + glucose + urea 2. Replace fluid and electrolyte losses * 0.9% saline 3-6 litres by 12 hours * Potassium added or omitted as required 3. Normalise blood glucose (gradually)
146
What are the complications of HHS?
1. Myocardial infarction 2. Stroke 3. Peripheral arterial thrombosis 4. Seizures 5. Cerebral oedema 6. Central pontine myelinolysis (CPM)
147
WHAT IS CARCINOID SYNDROME? What three symptoms are under the syndrome?
Specific type of tumour Causes neuroendocrine cells to secrete hormones * *_Syndrome_** * *D**iarrhoea * *F**lushing * *S**OB
148
Where are neuroendocrine cells found?
Epithelial layer of GI organs and lungs Kulchitsky cells Mid-gut Hind-gut
149
How are neuroendocrine cells activated and what can they release?
**_Nerves_** 1. Serotonin 2. Histamine 3. Bradykinin 4. Prostaglandins
150
What are symptoms of carcinoid syndrome worsened by?
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
151
What are the investigations for carcinoid syndrome?
1. **Urinalysis - FIRST LINE** * 5-hydroxyindoleacetic acid (5-HIAA) 2. **Plasma Chromogranin A (CgA) - SECOND LINE** 3. **Octreoscan** * Inject radioactive labelled octreotide * Binds to increase number of somatostatin 4. **Blood tests** * Niacin deficiency
152
What is the treatment for cacinoid syndrome?
1. **Somatostatin analogues** * Octreotide 2. **Carcinoid tumour** * Surgery * Chemo
153
WHAT IS DIABETES INSIPIDUS?
Lack of ADH
154
What happens from a lack of ADH?
Water not sufficiently reabsorbed from collecting duct Large amounts of undilute urine
155
What are the symptoms of diabetes insipidus?
1. Polydipsia 2. Polyuria 3. Dehydration 4. Hypernatremia
156
What is central and nephrotic diabetes insipidus?
1. **Central problem with hypothamus and pituitary** * ADH low 2. **Nephrotic problem with kidneys** * ADH high
157
What are the causes of central diabetes insipidus?
1. Tumour 2. Lack of blood supply (inc Sheehan’s) 3. Impact/fracture 4. Surgical 5. Autoimmune 6. Haemochromatosis
158
What are the nephrogenic causes of diabetes insipidus?
1. Lithium toxicity 2. Release of obstruction 3. Hypercalcemia 4. Hypokalaemia
159
What are the investigations for diabetes insipidus?
1. High plasma osmolality, low urine osmolality 2. A urine osmolality of \>700 mOsm/kg excludes diabetes insipidus 3. **Urine osmolality is AUTOMATICALLY LOW ANYWAY** 4. **Nephrogenic DI** * Water deprivation test * Low urine osmolality * Desmopressin * Low urine osmolality 5. **Cranial DI** * ​​Water deprivation test * Low urine osmolality * Desmopressin * High
160
How can you determine the cause of diabetes insipidus?
1. Give desmopressin 2. If urine output falls, osmolality increases 3. **Suggests central**
161
What is the treatment of diabetes insipidus?
1. **Central** * Desomopressin 5-40mg intranasally 2. **Diuretics** * Hydrocholorothiazide * Low salt/protein diet
162
Why do you give a patients diuretics with nephrotic diabetes insipidus?
Promote water AND SALT LOSS Activate RAAS!!
163
WHAT IS THE DIFFERENCE BETWEEN DIABETES INSIPIDUS VS SIADH?
164
WHAT DOES THE PARATHYROID DO? What does this hormone do?
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
165
What does the thyroid release in high levels of calcium? What does this do?
Calcitoin Increase bone deposition Decrease kidney absorption of calcium
166
WHAT IS HYPERPARATHYROIDISM?
Increase in parathyroid hormone
167
What are the different causes of hyperparathyroidism?
1. **Primary** * Solitary Adenoma - normal parathyroid * Hyperplasia 2. **Secondary** * PTH is high to attempt to correct persistently low calcium levels * CKD * Malabsorption and vitmain D deficiency 3. **Tertiary** * After many years of uncorrected secondary hyperparathyroidism
168
What are the symptoms of hyperparathyroidsm?
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.
169
What are the tests for primary hyperparathyroidism?
**_PTH_** High **_Calcium_** High **_Phosphate_** Low **_Phosphatase_** High
170
What is the treatment for primary hyperparathyroidism?
1. Parathyroidectomy - first choice if symptomatic 2. **Medical management** * Bisphosphonates
171
What are the tests for secondary hyperparathyroidism?
**_PTH_** High **_Calcium_** Low **_Phosphate_** High **_Phosphatase_** High
172
What is the treatment for secondary hyperparathyroidism?
Treat underlying cause Bisphosphonates
173
WHAT IS HYPOPARATHYROIDISM?
Low levels of parathyroid hormone
174
What are the causes of hypoparathyroidism?
1. **Primary** * AI * Congenital (Di George syndrome) 2. **Secondary** * Radiation * Surgery * Hypomagnesaemia
175
What are the features of hypoparathyroidism?
Hypocalcaemia SPASMODIC 1. Spasms 2. Trousseau’s on inflation of cuff 3. Anxious 4. Seixures 5. Chvostek’s – tap facial nerve over parotid – corner of mouth twitches.
176
What are the investigations for hypoparathyroidism?
1. **Low serum calcium** 2. **Increased plasma phosphate** - low in hypocalcaemia due to intestinal malabsorption or vitamin D deficiency 3. **Normal alkaline phosphatase** - raised in hypocalcaemia due to chronic renal failure 4. Skull radiology may reveal basal ganglia calcification 5. PTH: low plasma levels 6. urinary cAMP excretion rises following administration of PTH
177
What is the treatment of hypoparathyroidism?
1. **Acute symptomatic hypocalcaemia** * IV correction wioth calcium 2. **Vitamin D** 3. **Ca2+ supplements** * if diet is lacking 4. Calcitriol (prevents hypercalciuria)
178
What is the treatment for postmenopausal woman who have a fracture?
Risedronate and calcium supplements
179
WHAT IS PHAEOCHROMOCYTOMA?
Catecholamine secreting tumour
180
What are the clinical features of phaeochromocytoma?
1. hypertension (around 90% of cases, may be sustained) 2. headaches 3. palpitations 4. sweating 5. anxiety
181
What are the investigations for phaeochromocytoma?
1. 24 hr urinary collection of **metanephrines** * This replaced 24hr collection of catecholamines
182
What is the management for phaeochromocytoma?
1. Surgery is **definitive** 2. Alpha-blocker (e.g. **phenoxybenzamine**) before 3. Beta-blocker (e.g. **propranolol**)
183
WHAT HORMONES ARE INCREASED AFTER SURGERY?
1. Growth hormone 2. Cortisol 3. Renin 4. Adrenocorticotrophic hormone (ACTH) 5. Aldosterone 6. Prolactin 7. Antidiuretic hormone 8. Glucagon
184
What hormones are decreased following surgery?
1. Insulin 2. Testosterone 3. Oestrogen
185
What hormones have no change after surgery?
1. Thyroid stimulating hormone 2. Luteinizing hormone 3. Follicle stimulating hormone
186
WHAT IS SICK EUTHYROID SYNDROME?
1. In sick euthyroid syndrome (now referred to as non-thyroidal illness) it is often said that everything (TSH, thyroxine and T3) is low. 2. In the majority of cases however the TSH level is within the \>normal range
187
What is the treatment for sick euthyroid syndrome?
Changes are reversible upon recovery from the systemic illness and hence no treatment is usually needed
188
WHAT ARE THE SIDE EFFECTS OF STEROIDS?
1. endocrine: impaired glucose regulation, increased appetite/weight gain, hirsutism, hyperlipidaemia 2. Cushing's syndrome: moon face, buffalo hump, striae 3. musculoskeletal: osteoporosis, proximal myopathy, avascular necrosis of the femoral head 4. immunosuppression: increased susceptibility to severe infection, reactivation of tuberculosis 5. psychiatric: insomnia, mania, depression, psychosis 6. gastrointestinal: peptic ulceration, acute pancreatitis 7. ophthalmic: glaucoma, cataracts 8. dermatological: acne 9. suppression of growth in children 10. intracranial hypertension 11. neutrophilia
189
WHAT IS A PROLACTINOMA?
Prolactinomas are a type of pituitary adenoma, a benign tumour of the pituitary gland
190
What are pituitary adenomas classified by?
1. Size (a microadenoma is \<1cm and a macroadenoma is \>1cm) 2. Hormonal status (a secretory/functioning adenoma produces and excess of a particular hormone and a non-secretory/functioning adenoma does not produce a hormone to excess)
191
What are the features of prolactinomas?
1. Excess prolactin in women * amenorrhoea * infertility * galactorrhoea * osteoporosis 2. Excess prolactin in men * impotence * loss of libido * galactorrhoea 3. Other symptoms may be seen with macroadenomas * headache. * visual disturbances (classically, a bitemporal hemianopia (lateral visual fields) or upper temporal quadrantanopia) * symptoms and signs of hypopituitarism
192
How is a prolactinoma diagnosed?
MRI
193
What is the management of a prolactinoma?
1. In the majority of cases, symptomatic patients are treated medically with dopamine agonists **(e.g. cabergoline, bromocriptine)** which inhibit the release of prolactin from the pituitary gland 2. Surgery is performed for patients who cannot tolerate or fail to respond to medical therapy. A **trans-sphenoidal** approach is generally preferred unless there is a significant extra-pituitary extension
194
WHAT ARE THE MANAGEMENT OPTIONS FOR OBESITY?
1. Conservative: diet, exercise 2. Medical 3. Surgical
195
What is orlistat?
Pancreatic lipase inhibitor
196
WHAT IS CONGENITAL ADRENAL HYPERPLASIA?
1. Group of autosomal recessive disorders 2. Affect adrenal steroid biosynthesis 3. In response to resultant low cortisol levels the anterior pituitary secretes high levels of ACTH 4. ACTH stimulates the production of adrenal androgens that may virilize a female infant
197
What are the causes of congenital adrenal hyperplasia?
1. 21-hydroxylase deficiency (90%) 2. 11-beta hydroxylase deficiency (5%) 3. 17-hydroxylase deficiency (very rare)
198
WHAT IS PEUTZ-JEGHERS SYNDROME?
Peutz-Jeghers syndrome is an autosomal dominant condition characterised by numerous hamartomatous polyps in the gastrointestinal tract. It is also associated with pigmented freckles on the lips, face, palms and soles. Although the polyps themselves don't have malignant potential, around 50% of patients will have died from another gastrointestinal tract cancer by the age of 60 years.
199
What are the features of peutzs-jeghers syndrome?
1. hamartomatous polyps in GI tract (mainly small bowel) 2. pigmented lesions on lips, oral mucosa, face, palms and soles 3. intestinal obstruction e.g. intussusception 4. gastrointestinal bleeding
200
WHAT IS KLINEFELTER'S SYNDROME?
Klinefelter's syndrome is associated with karyotype 47, XXY.
201
What are the features of Klinefelter's syndrome?
1. often taller than average 2. lack of secondary sexual characteristics 3. small, firm testes 4. infertile 5. gynaecomastia - increased incidence of breast cancer 6. elevated gonadotrophin levels but low testosterone
202
How do you diagnose klinefelter's syndrome?
Karyotype
203
WHAT IS WATERHOUSE-FRIDERICHSEN SYNDROME?
1. Adrenal gland haemorrhage 2. Profound sepsis 3. Coagulopathy
204
WHAT IS MATURITY-ONSET DIABETES?
1. Maturity-onset diabetes of the young (MODY) is characterised by the development of type 2 diabetes mellitus in patients \< 25 years old. 2. It is typically inherited as an autosomal dominant condition. 3. Over six different genetic mutations have so far been identified as leading to MODY.
205
WHAT IS THE TREATMENT OF HYPERTHYROID IN PREGNANCY?
Propylthiouracil
206
WHAT IS BARTONELLA INFECTION?
Bartonella infection may occur following a cat scratch. The organism is intracellular. Generalised systemic symptoms may occur for a week or so prior to clinical presentation.
207
WHAT ARE THE CAUSES OF HYPOPITUITARISM?
1. compression of the pituitary gland by non-secretory pituitary macroadenoma (most common) 2. pituitary apoplexy 3. Sheehan's syndrome: postpartum pituitary necrosis secondary to a postpartum haemorrhage 4. hypothalamic tumours e.g. craniopharyngioma 5. trauma 6. iatrogenic irradiation 7. infiltrative e.g. hemochromatosis, sarcoidosis
208
What are the symptoms of hypopituitism?
1. low ACTH * tiredness * postural hypotension 2. low FSH/LH * amenorrhoea * infertility * loss of libido 3. low TSH * feeling cold * constipation 4. low GH * if occurs during childhood then short stature 5. low prolactin * problems with lactation 6. there may also be features suggestive of the underlying causes * pituriary macroadenoma → bitemporal hemianopia * pituitary apoplexy → sudden, severe headache
209
What are the investigations for hypopituitism?
1. hormone profile testing 2. imaging
210
What is the management of hypopituitarism?
1. treatment of any underlying cause (e.g. surgical removal of pituitary macroadenoma) 2. replacement of deficient hormones

ΩΩ 4 Bateman - Specialities + Endo + GI + Liver (6 decks)

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