Endocrinology Flashcards

(153 cards)

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.

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

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

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

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

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

What are the complications of acromegaly?

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

Vascular
HTN
LVH
Cardiomyopathy
Arrhythmias

Colon cancer

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

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

What is the treatment of acromegaly?

A

Trans-sphenoidal Surgery

Radiation

Medications - suppress GH
Somatostatin anaologues
Octreotide

Recombinant GH receptor antagonist
Pegvisomant

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

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

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

A

Zona glomerulosa

Zona fasiculata

Zona reticularis

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

What is the zona festiculata?

A

Largest zone

Stimulate cells in this zone to secrete cortisol

Cortisol is a glucocorticoids

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

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

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

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

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

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

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

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

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

A

Nelson’s syndrome

Skin pigmentation increase

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

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

What are the symptoms caused by in SIADH?

A

Derived from decreased sodium in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?
Primary atrophic hypothyroidism (No goitre) Hashimoto’s thyroiditis (Goitre) Iodine deficiency Post-thyroidectomy / radioiodine / antithyroid drugs 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?
**_TFT_** TSH RAISED **_Lipids/cholesterol_** High **_FBC_** Macrocytosis
35
What are the disease associations of hypothyroidism?
**_AUTOIMMUNE_** Type 1 Diabetes Mellitus Addison’s disease Pernicious anaemia Primary biliary cirrhosis **_INHERITED_** Turner’s syndrome Down’s syndrome Cystic fibrosis
36
What is the treatment of hypothyroidism?
Levothyroxine (T4) Higher doses in the young
37
WHAT IS HASHIMOTO's THYROIDITIS? | (inside hypothyroidism)
Autoimmune disease T cell mediated attack
38
What are the symptoms of hasimoto's thyroiditis?
Goitre or hypothyroidism or both Enlargement is usually slow and painless but rarely, may be more rapid and painful
39
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 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
40
What is the treatment of hasimoto's thyroiditis?
If the patient is hypothyroid then oral thyroxine may keep the patient euthyroid and lead to resolution of the goitre.
41
WHAT IS HYPERTHYROIDISM?
Too much thyroid hormones
42
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)
43
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
44
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
45
What are the investigations for hyperthyroidism?
**_TFT_** Increase T4 and T4 **_FBC_** Normocytic anaemia **_ESR (↑)_** **_Calcium (↑)_** **_LFT (↑)_** **_Thyroid autoantibodies_** **_Visual fields, acuity, eye movements_**
46
What is the treatment for hyperthyroidism?
**_β-blockers_** Propanolol(rapid control of symptoms) **_Antithyroid medication_** Carbimazole SE = AGRANULOCYTOSIS Block and replace (carbimazole + thyroxine) **_Radioiodine (131I)_** **_Thyroidectomy_**
47
What happens in graves disease? What are the triggers?
Autoimmune IgG autoantibodies bind to and stimulate TSH receptors Infection, stress, childbirth
48
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!!
49
What are the investigations for Grave's disease?
* 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
50
What is the treatment of Grave's disease?
1. Radioactive iodine - first-line 2. Carbimazole 3. Thyroidectomy
51
What are some causes of goitre?
Physiological Graves’ disease Hashimoto’s thyroiditis De Quervain’s
52
WHAT ARE THE MOST LIKELY THYROID CELL TYPE CANCERS?
Papillary (60%) Follicular (≤25%) Medullary (5%) Lymphoma (5%) Anaplastic
53
What are some causes of thyroid cancer?
Low dose radiation Radioiodine A history of radiation exposure to the neck area is associated with increased risk of thyroid cancer
54
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.
55
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
56
What is the treatment for thyroid cancer?
Most thyroid tumours are treated surgically with follow up radioiodine ablation
57
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
58
What are the different layers of the adrenal glands?
**_Cortex_** Zona glomerulosa Zona fasiculata Zona reticularis **_Medulla_**
59
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
60
What does the renin, angiotensin aldosterone system do?
Decrease potassium Increase sodium Increase blood volume and pressure
61
What are the causes of primary adrenal insuffiency?
In developed countries **_Autoimmune destruction_** Unclear reason Developing countries **_Tuberculosis_** Infection spreads from lungs to adrenal glands **_Metastatic carcinoma_**
62
What happens if the zona glomerulosa is destroyed?
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
What are the symptoms if the zona glomerulosa is affected?
Cravings for salty foods Nausea and vomiting Fatigue Dizzyness
64
What are the symptoms if the zona fasiculata is destroyed?
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
What are the symptoms if the zona fasiculata is destroyed?
Fatigue in times of stress Hyperpigmentation on knuckles and joints
66
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
67
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
68
How can you diagnose addison's disease?
**_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
What is the treatment for addison's disease?
Homones Cortisol - hydrocortisone Aldosterone - Fludrocortisone Androgens Take for life Stopping can lead to crisis
70
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
71
What is it called when the body suddenly needs aldosterone or cortisol and the body can't deliver?
Addisonian crisis (acute primary adrenal insufficiency)
72
What syndrome can cause an addisonian crisis?
Waterhouse-friderichsen syndrome Causes blood vessels in adrenal glands to rupture
73
What are the symptoms of addisonian crisis?
Pain in back abdomen or legs Vomiting and diarrhoea leading to dehydration Low blood pressure leading to loss of consciousness Death
74
WHAT IS SECONDARY ADRENAL INSUFFICIENCY?
Lack of ACTH and therefore cortisol
75
What are the causes for secondary adrenal insufficiency?
**_Medications_** Glucocorticoids Pituitary mass or infection
76
Why is aldosterone unaffected in secondary adrenal insufficiency?
Aldosterone secretion independent of ACTH
77
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: 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
What is the diagnosis of secondary adrenal insufficiency?
**_Bloods_** Low cortisol
79
What is the treatment for secondary adrenal insufficiency?
**Glucocorticoid analogues - hydrocortisone** 10mg in morning, 5 mg at midday, 5mg in evening. **Fludrocortisone**
80
WHAT IS CONN'S SYNDROME? https://www.youtube.com/watch?v=JBfkGNr01V8&t=1s
Hyperaldosteronism
81
What is the cause of Conn's syndrome?
Adrenal adenima Bilteral adrenal nodular hyperplasia
82
If there is high aldosterone levels, what will the ion levels be in the blood?
Potassium low Sodium high Less protons
83
What do the ions in the blood in conn's syndrome cause?
Hypertension Metabolic alkolosis
84
What are the symptoms of Conn's syndrome?
Headaches and flushing Constipation Weakness Heart rhythm changes
85
What is the diagnosis of Conn's syndrome?
**_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
What is the treatment for Conn's syndrome?
**_Potassium sparing diuretic_** Spirinolactone **_Surgery_** Remove tumour
87
WHAT DIABETES MELLITUS?
Trouble moving glucose from blood into cells High level in blood Not alot in cells
88
What are the different types of diabetes?
Type 1 10% Type 2 90%
89
What is the cause of type 1 diabetes?
Bodies own cells attack the pancreas Type 4 hypersensitivty reaction Cell-mediated response
90
What are the symptoms of type 1 diabetes?
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
What are some complications of diabetics with bad control?
Vascular disease Nephropathy Neuropathy Diabetic foot Retinopathy
92
What are the investigations for type 1 diabetes?
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
What is the treatment for type 1 diabetes?
Lifelong insulin injections Education
94
What is are the diabetic emergencies?
Hypoglycaemia Hyperglycaemia Diabetic ketoacidosis Hyperosmolar non-ketotic hyperglycemia
95
WHAT IS DIABETIC KETOACIDOSIS?
Biochemical triad of 1. Ketonaemia 2. Hyperglycaemia 3. Acidaemia
96
What can ketones do to the blood?
Make the blood acidic Kussmaul respiration Deep/labored breathing To reduce CO2 Reduce acidity
97
How can a diabetic ketoacidosis happen in somebody who already has insulin treatment?
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
What are the symptoms of diabetic ketoacidosis?
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
What do the ketone bodies break down into? What does this cause to the breath?
Acetone Fruity smell
100
What does ketoacidosis cause?
Nausea Vomiting Mental status changes Cerebral oedema
101
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
102
What is the diagnosis of DKA?
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
What is the treatment for diabetic ketoacidosis?
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
WHAT IS TYPE 2 DIABETES MELLITUS?
Body makes insulin but the cells don't respond Not fully understood
105
What are the risk factors for type 2 diabetes?
Obesity Lack of exercise Hypertension
106
What is normoglycemia?
Insulin levels high when cells don't respond to insulin Blood glucose levels remain normal
107
What are the symptoms of type 2 diabetes mellitus?
polydipsia polyuria, with associated nocturia or enuresis glycosuria
108
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
109
What is the management of diabetes type 2?
1. Metformin 2. SU - e.g. Glipizide 3. DPP-4i - GLIPTINS 4. Pioglitazone 5. SGLT-2i - GLIFLOZINS
110
What systemic problems can diabetes cause?
Retinopathy Kidneys Nephrotic syndrome Nerves Decrease in sensation Stocking-glove distribution
111
How does metofrmin 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
112
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
113
How do DDP-4i work?
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
What is the difference between diabetes type 1 and diabetes type 2?
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
WHAT IS HYPERGLYCEMIC HYPEROSMOLAR STATE?
Extreme elevations in serum glucose concentrations, hyperosmolality and dehydration without significant ketosis
116
What are the clinical features of HHS?
Hyperglycaemia Dehydration with marked thirst Marked drowsiness Weakness Visual disturbance Leg cramps Nausea and vomiting - less frequent than in patients with DKA
117
What is the diagnostic criteria for HHS?
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
What is the management of HHS?
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
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
120
Where are neuroendocrine cells found?
Epithelial layer of GI organs and lungs Kulchitsky cells Mid-gut Hind-gut
121
How are neuroendocrine cells activated and what can they release?
**_Nerves_** 1. Serotonin 2. Histamine 3. Bradykinin 4. Prostaglandins
122
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
123
What are the investigations for carcinoid syndrome?
**_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
What is the treatment for cacinoid syndrome?
**_Somatostatin analogues_** Octreotide **_Decrease_** Emotional stress Alcohol **_Carcinoid tumour_** Surgery Chemo
125
WHAT IS DIABETES INSIPIDUS?
Lack of ADH
126
What happens from a lack of ADH?
Water not sufficiently reabsorbed from collecting duct Large amounts of undilute urine
127
What are the symptoms of diabetes insipidus?
1. Polydipsia 2. Polyuria 3. Dehydration 4. Hypernatremia
128
What is central and nephrotic diabetes insipidus?
**_Central problem with hypothamus and pituitary_** ADH low **_Nephrotic problem with kidneys_** ADH high
129
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
130
What are the nephrogenic causes of diabetes insipidus?
1. Lithium toxicity 2. Release of obstruction 3. Hypercalcemia 4. Hypokalaemia
131
How can you determine the cause of diabetes insipidus?
Give desmopressin If urine output falls, osmolality increases Suggests central
132
What is the treatment of diabetes insipidus?
**_Central_** Desomopressin 5-40mg intranasally **_Diuretics_** Hydrocholorothiazide
133
Why do you give a patients diuretics with nephrotic diabetes insipidus?
Promote water AND SALT LOSS Activate RAAS!!
134
WHAT IS THE DIFFERENCE BETWEEN DIABETES INSIPIDUS VS SIADH?
135
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
136
What does the thyroid release in high levels of calcium? What does this do?
Calcitoin Increase bone deposition Decrease kidney absorption of calcium
137
WHAT IS HYPERPARATHYROIDISM?
Increase in parathyroid hormone
138
What are the different causes of hyperparathyroidism?
**_Primary_** Adenoma **_Secondary_** PTH is high to attempt to correct persistently low calcium levels **_Tertiary_** After many years of uncorrected secondary hyperparathyroidism
139
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.
140
What are the tests for primary hyperparathyroidism?
**_PTH_** High **_Calcium_** High **_Phosphate_** Low **_Phosphatase_** High
141
What is the treatment for primary hyperparathyroidism?
Treat underlying cause
142
What are the causes of secondary hyperparathyroidism?
**_CKD_** **_vit D deficiency_** GI disease such as bypass and Crohn’sare also possible
143
What are the symptoms for hyperparathyroidism?
Bony Osteomalacia
144
What are the tests for secondary hyperparathyroidism?
**_PTH_** High **_Calcium_** Low **_Phosphate_** High **_Phosphatase_** High
145
What is the treatment for secondary hyperparathyroidism?
Treat underlying cause Bisphosphonates
146
WHAT IS HYPOPARATHYROIDISM?
Low levels of parathyroid hormone
147
What are the causes of hypoparathyroidism?
**_Primary_** AI, congenital (Di George syndrome) **_Secondary_** Radiation, surgery, hypomagnesaemia
148
What are the signs of hypoparathyroidism?
Hypocalcaemia SPASMODIC Spasms Trousseau’s on inflation of cuff anxious seixures Chvostek’s – tap facial nerve over parotid – corner of mouth twitches.
149
What is the treatment of hypoparathyroidism?
Ca2+ supplements Calcitriol (prevents hypercalciuria)
150
WHAT IS PHAEOCHROMOCYTOMA?
Catecholamine secreting tumour
151
What are the clinical features of phaeochromocytoma?
hypertension (around 90% of cases, may be sustained) headaches palpitations sweating anxiety
152
What are the investigations for phaeochromocytoma?
24 hr urinary collection of metanephrines replaced 24hr collection of catecholamines
153
What is the management for phaeochromocytoma?
1. Surgery is definitive 2. Alpha-blocker (e.g. **phenoxybenzamine**) before 3. Beta-blocker (e.g. **propranolol**)