Endocrine Flashcards
(219 cards)
1
Q
Give a simple definition of type 1 diabetes
A
Autoimmune destruction of the pancreatic beta cells –> complete insulin deficiency
2
Q
What type of hypersensitivity reaction is T1DM?
A
4
3
Q
What are 3 risk factors for T1DM
A
Northern European
Other autoimmune diseases e.g. coeliac, rheumatoid arthritis
Gene mutations/ variants
4
Q
Which specific genes may be different in T1DM and where are they found (what cell)
A
HLA DR3-DQ2
HLA DR4-DQ8
Found on Beta cells (they express HLA genes)
5
Q
Epidemiology of T1DM (3 things)
A
Age usually 5-15
BMI < 25
10% of all diabetes
6
Q
How does T1DM cause hyperglycaemia?
A
B cells attacked –> insulin deficiency –> gluconeogenesis, glycogenlysis, decreased cell uptake of glucose
7
Q
How does T1DM cause hyperkalemia (in blood)?
A
Insulin stimulates Na+/K+ ATPase pumps, therefore lack of insulin means K+ can’t get in cells
8
Q
How is T1DM diagnosed?
A
RPA > 11.1 mmol/l
FPG > 7 mol/l
HbA1C >48 mol/l or 6.5%
9
Q
Signs/ symptoms of T1DM (3)
A
Polydipsia
Polyuria
Weight loss (can’t get glucose in cells)
10
Q
Treatment of T1DM
A
SC fat insulin injection
11
Q
Rapid acting insulin name
A
aspart
12
Q
Short acting insulin name
A
regular insulin
13
Q
Intermediate acting insulin name
A
NPH (Neutral protamine hagedorn)
14
Q
Long acting insulin name
A
Glargine
15
Q
What is DKA (simple)
A
Complication of diabetes (usually type 1) where lack of insulin = high ketone levels, acidosis and hyperglycaemia
16
Q
Pathology of DKA (hyperglycaemia, acidosis and high ketone levels)
A
No insulin –> hyperglycaemia (but cells starved of glucose) –> lipolysis/ ketogenesis –> increase in ketones in blood –> acidosis (initially buffered by bicarbonate)
17
Q
What might bring on DKA
A
Illness/ infection
18
Q
Symptoms of DKA (4)
A
Diabetes symptoms
Nausea/ vomiting
Confusion/ drowsiness
Abdo pain (liver stretches)
19
Q
Signs of DKA (4)
A
Kussmaul breathing (deep+fast to expel CO2)
Pear drop breath
Hypotension (hypovolaemic)
Tachycardia
20
Q
Diagnosis of DKA
A
RPG > 11 mmol/l
Plasma ketones > 3 mmol/l
Blood pH < 7.35 or Bicarb < 15 mmol/l
21
Q
Treatment of DKA
A
- ABC (emergency)
- Fluids (0.9% saline)
- IV regular insulin and K+
22
Q
Why is K+ essential to treat DKA with
A
Insulin makes K+ enter cells therefore K+ will immediately enter cells when insulin administered, so K+ in the blood must be restored to prevent cardiac arrest
23
Q
Complications of DKA (3)
A
Coma/ death
Cerebral oedema
Aspiration pneumonia
24
Q
What is T2DM (simple)
A
Peripheral insulin resistance and may lead to insulin deficiency
25
Pathology of T2DM
Repeated insulin exposure --> insulin resistance --> more insulin required for response --> beta cells grow tired + stop working --> insulin deficiency
26
T2DM risk factors (6)
Age (30+)
Male
Obesity
Sedentary
African or South Asian
Genetics
27
Signs + symptoms of T2DM (7)
Fatigue
Polydipsia + polyuria
Glucosuria
Slower onset > 6 months
Central obesity
Slow healing + infections (bad circulation)
Blurred vision (once progressed)
28
Diagnoses of T2DM (4 ways) and diagnostic values
Fasting plasma glucose = after 8 hours
Oral glucose tolerance test = 75g glucose drink after fast then measure glucose level 2 hours later
29
What are the 5 steps to manage T2DM
1. Lifestyle changes
2. Metformin
3. Double therapy
4. Triple therapy
5. Insulin
30
What class of drug is metformin
Biguanide
31
How does Metformin work (2)
* Decrease liver gluconeogenesis
* Increase cell sensitivity to insulin
32
Metformin side effects (2)
* GI disturbances
* lactic acidosis, as no gluconeogenesis. (can be serious)
33
What can metformin be used in combination with (4)
* DPP 4 inhibitors
* Sulfonylurea - cause Beta cells to make more insulin (glicazide)
* Pioglitazone - improve insulin sensitivity
* SGLT-2 inhibitors
34
What is hyperosmolar hyperglycaemic state (simple)
Hyperglycaemia without ketosis
35
What is the pathophysiology of HHS how does it cause hyperglycaemia and dehydration?
Low insulin --> hyperglycaemia
(Insulin not absent therefore ketogenesis does not occur)
Hyperglycaemia --> glucose sucks water out of blood --> dehydration
36
What may bring on HHS in those with diabetes?
Infection/illness
37
Signs/ symptoms of HHS (4)
* Diabetes symptoms
* Confusion
* Dehydration
* Lethargy
38
Investigations for HHS (4)
* RPG = high
* Urine dipstick = glycosuria
* Plasma osmolality > 320 mOsm/kg
* No ketones in urine
39
Treatment for HHS
1. Fluid replacement (0.9% saline)
2. Insulin - slow infusion; with K+
40
What is diabetes insipidus (simple)
A lack of ADH **or** a lack of response to ADH
41
What are the 2 types of DI
* Nephrogenic - collecting ducts don't respond to ADH
* Cranial - impaired production/ secretion from hypothalamus/ post. pituitary
42
Where does ADH take effect and what channel does it effect?
* V2 receptor - increases expresion of AQ2 in collecting ducts of kidneys; increases reabsorption of Na+ in the collecting ducts.
* V1 receptor - causes vasoconstriction
43
Where is AQ1 found
Proximal convoluted tubules and descending limb of LoH
44
What is primary polydipsia
Some idiot drinking too much
45
What causes nephrogenic DI (4)
* Drugs (e.g. lithium for BPD)
* Renal disease
* Electrolyte imbalances (damage nephrons)
* Congential/ inherited/ mutation
46
What causes cranial DI (5)
* Idiopathic
* Brain tumours
* Head injury
* Congential/ mutation
* Infection (meningitis)
47
Signs/ symptoms of DI (4)
* polyuria/ polydipsia
* dehydration
* Postural hypotension
* Hypernatraemia (hypovolemic)
48
How much urine is suspicious of DI
3 litres in 24 hours
49
What is the diagnostic test for DI and describe it
Water deprivation test:
* no fluids 8 hours - measure urine osmolality
* give synth. ADH - measuere urine osmolality 8 hours later
50
What are the expected results of water deprevation test for cranial DI, nephrogenic DI and pimary polydipsia
51
What other investigations may be done for DI (3)
* Urine dip
* U&Es
* Cranial MRI (check for tumours...)
52
Compliactions of DI (2)
* Dehydration
* Electrolyte imbalance
53
Treatment for DI
Treat underlying cause
* rehydration for mild
* Cranial - desmopressin
* Nephrogenic - thiazide diuretic: bendroflumethiozide
54
How do thiazide diuretics work
Block Na-Cl co-transporters and blarrrrr blarrrrr blarrrrrrrrr
But nobody has a fucking clue
55
What is syndrome of inappropriate ADH (simple)
Large amounts of ADH cause excess fluid to be reabsorbed in collecting duct
56
Pathophysiology of SIADH - how does it cause excess reabsorption of water
Excess ADH is produced/ secreted--> increase expression of AQ2 in collecting duct --> increased reabsorption of water
57
Why does euvolaemic hyponatraemia occur in SIADH
Sodium is excreted from kidneys to compensate for the over reabsorption of water. As water follows sodium the correct fluid volume is maintained, however the body is low in sodium.
58
What causes SIADH (4)
* Infection
* Head injury
* Medications
* Tumours (secrete ADH)
59
Which tumours can secrete ADH (5)
* SCLC
* Prostate
* Thymus
* Pancreatic
* Lymphomas
60
Which medications cause SIADH (3)
* Thiazide diuretics
* NSAIDs
* SSRIs
61
What are the symptoms of SIADH (4), (signs in next card)
* N+V
* Headache
* Fatigue
* confusion
| siezures + reduced consiousness more severe symptoms of hyponatraemia
62
What are the signs of SIADH (3)
* Raised jugular vein pressure
* Oedema
* Ascites
63
How is SIADH diagnosed
It is a diagnosis of exclusion
* U&E --> hyponatraemia and normal K
* Urine sodium + osmolality = high
| Exclude other causes of hyponatraemia e.g. CKD, diuretic use...
64
How is SIADH managed (what medicine is used)
1. Treat cause
2. Fluid restriction
3. Tolvaptan - ADH receptor antagonist; Furosemide - strong diuretic
65
What are some complications of SIADH (4)
* Cerebral oedema
* Siezures
* Coma
* Central pontine myelinolysis
66
How does SIADH cause central pontine demyelinolysis
Na+ low in blood --> solutes move out of brain to prevent cerebral oedema
*Hyponatraemia treated too quickly*
Blood Na+ rises quickly --> water moves out of brain quickly --> demyelination of neuones
67
What is Cushing's syndrome (simple)
Chromic excess of cortisol
68
Where is cortisol released from
zona fasiculata of the adrenal gland
69
Describe the HPA axis
Hypothalamus releases corticotropin releasing hormone --> anterior pituitary releases adrenocorticotropin releasing hormone --> adrenal gland releases cortisol
| This is regulated by negative feedback
70
Cortisol actions in body (5)
* Inhibits immune system
* Increases blood glucose
* Increases alertness
* Increases metabolism
* Inhibits bone formation
| All more long term flight/ fight responces
71
Causes of cushing's ACTH dependant (2)
* Cushings disease - pituitary adenoma releases ACTH --> adrenal hyperplasia
* Ectopic ACTH - from SCLC
72
Causes of Cushing's ACTH independant (2)
* Adrenal adenoma - secretes cortisol
* Iatrogenic steroid use (corticosteroids)
| iatrogenic = caused by medical procedure or treatment
73
What are the sign and symptoms of Cushing's (5)
* Moon face (round)
* Central obesity
* Buffalo hump (fat on shoulders)
* Abdominal striae
* Osteoporosis
74
How is Cushing's syndrome investigated
* Random plasma cortisol levels, if abnormal...
* Dexamethasone suppression test, if abnormal...
* Plasma ACTH
75
How is random plasma cortisol levels different in those with cushing's
Does not follow typical diurnal pattern (high in morning, low at night)
And generally higher overall
76
What is dexamethasone
Binds to same receptors as cortisol (therefore inhibits ACTH)
77
Describe how the low dose dexamethasone supression test works
1 mg DM given @10pm --> cortisol measured @9am
Low cortisol = normal
High/ normal cortisol = cushing's
78
Describe how the high dose dexamethasone supression test works
8mg DM given @10pm --> ACTH and cortisol measued @9am
**Low** cortisol = cushings disease (-ve feedback in high dose able to suppress pit adenoma)
**High**/ **normal** cortisol and **low** ACTH = adrenal adenoma
**High/ normal** cortisol and **high** ACTH = ectopic ACTH tumour
79
How is Cushing's treated (2)
* Treat/ stop underlying cause (excise tumour/ stop meds)
* Remove adrenal glands and give steroidal treatment
80
What are some compliactions of cushing's (3)
* Diabetes (cortisol increases blood glucose so cells can become resistant to insulin)
* Hypertension/ CVD
* Osteoporosis
81
What is adrenal insufficiency (simple)
Adrenal glands dont produce enough steroid hormones (cortisol and aldosterone)
82
What are the two types of adrenal insufficiency
* Primary AI (Addison's disease) = adrenal cortex damaged
* Secondary AI = pituitary/ hypothalamic involvement (low ACTH/ CRH)
83
Pathophysiology of two types of adrenal insufficiency
Primary - adrenal gland damaged = low steroids --> hight ACTH to try to compensate
Secondary - low CRH/ACTH --> low steroidal hormones
84
What are some causes of Addison's disease (2)
* Autoimmune destruction - 80% of cases in UK
* TB infection - damages adrenal gland
85
What antibody is often present in those with Addison's
21-hydroxylase antibody
86
What causes secondary AI (5)
* Surgery
* Infection e.g. meningitis
* Radiotherapy
* Necrosis
* Iatrogenic - supression of HPA
87
What are some symptoms of AI (5)
* Fatigue/ weakness
* Weight loss
* Nausea
* Decreased libido
* Change in body hair
| (Dermatological stuff in the signs card)
88
What are some signs of AI
* Dermatological - hyperpigmentation and vitiligo
* Hypoglycaemia
* Postural hypotension
89
What causes hyperpigmentation in AI and therefore which type is affected
ACTH stimulates melanocytes to produce melanin
Therefore occurs in primary AI as lots of ACTH produced to compensate for damaged adrenal gland
90
What is a severe presentation of AI known as and what are the symptoms/ signs (3)
Addisonian/adrenal crisis
* reduced consciousness
* hypotension
* low NA+, hypoglycaemia, high K+
91
How is adrenal insufficiency investigated (2)
1st line: U&Es --> low sodium, high potassium, hypoglycaemia
Gold: short syncathen test
| 21-hydroxylase autoABs test
92
How does the short syncathen test work
Syncathen (synthetic ACTH) is administered --> cortisol levels monitored @baseline, 30 min and 60min --> if cortisol doesn't increase by much (doesn't double) = Addisons
93
How can secondary AI be diagnosed
Cortrosyn (synthetic CRH) administered --> affect an ACTH monitored
94
How is AI treated (name sof meds)
* Hydrocortisone (glucocorticoid) - to replace cortisol
* Fludrocortisone (mineralcorticoid) - to replace aldosterone
95
What should you do to AI medication during illness/ trauma
Double the dose to mimic stress responce
96
What is phaeochromocytoma (simple)
Tumour of the chromaffin cells of the adrenal medulla that secrete catecholamines
97
What pattern is adrenaline usually secreted in (for people with phaeochromocytoma)
Secreted in bursts, so periods of worse symptoms followed by settled periods
98
Which hormones are catecholamines (3)
* Adrenaline
* Noradrenaline
* Dopamine
99
What condition are phaeochromocytoma associated with
Multiple endocrine neoplasia type 2 (MEN type 2)
100
What is the pattern of phaeochromocytoma tumours (4 things)
* 10% bilateral
* 10% outside adrenal glands
* 10% cancerous
* 25% familial
101
What are the symptoms of phaeochromocytoma (think adrenaline) (4)
* Headache
* Sweating
* Cardiac - palpitations, tachycardia
* Tremor
102
What are some signs of phaeochromocytoma (2)
* Hypertension (hypertensive retinopathy)
* Pallor (looking pale)
103
How are phaeochromocytoma investigated
* Plasma metanephrines/ normetanephrines
* 24 hour urine catecholamines
* CT - look for tumour
104
What are metanephrines and why are they measured
Metabolites of adrenaline
They have a longer half life so less prone to fluctuation
105
How is phaeochromocytoma treated
* Medication (alpha/ beta blockers)
* Adrenalectomy = definitive treatment
106
What medication is used to treat phaeochromocytoma
* Alpha blocker - blocks noradrenaline
* Beta blocker - blocks adrenaline (prevents reactive vasoconstriction)
107
What is an example of an alpha blocker used in phaeochromocytoma?
Phenoxybenzamine
108
What is an example of a beta blocker
Atenolol
109
How is a hypertensive crisis treated in pheochromocytoma?
Phentolamine (antihypertensive alpha blocker)
110
What defines a hypertensive crisis
120/180
111
What is primary hyperaldosteronism (simple)
Overproduction of aldosterone idependant of the RAAS system
112
What causes primary hyperaldosteronism (2)
* Adrenal adenoma (Conn's syndrome)
* Bilateral adrenal hyperplasia
113
What is the pathophysiology of primary hyperaldosteronism (how are electrolytes affected)
More aldosterone produced --> high NA+ **reabsorption**, high H2O **reabsorption**, high K+ **excretion**
114
What are the signs/ symptoms of Conn's (4)
* Hypertension
* Electrolyte disturbance - arrhythmias, cramps, mood changes...
* Fatigue
* Polyuria/dipsia - low K+ interferes with kidney function
115
How is primary hyperaldosteronism investigated
* Low plasma K+
* Aldosterone high, renin low blood test
116
How is primary hyperaldosteronism treated
* Adrenalectomy for adenomas
* Aldosterone antagonist for bilateral hyperplasia
117
What is an example of an aldosterone antagonist
Spironolactone
118
What is secondary hyperaldosteronism
High rennin --> high aldosterone
(Not ACTH because this is Cushing's disease)
119
What usually causes secondary hyperaldosteronism
Disproportionatly low renal BP
(low renal BP)
120
What is hyperthyroidism (simple)
Excess thyroid hormones
121
What is the pathophysiology of hyperthyroidism (2 types)
* Primary - thyroid produces excess T3/4 independant of TSH
* Secondary - thyroid produces excess T3/4 due to overstimulation by TSH
122
Which thyroid hormone is active
T3 = triiodothyronine
123
What are the effects of T3 (4)
* Increase metabolism
* Activates SNS
* Increases bone resporption
* Increases cardiac output
124
Who is mainly affected by hyperthyroidism
Women, 20-40 yrs
125
What is the prevelance of Grave's disease in the population
0.5%
126
What causes primary hyperthyroidism (4)
* Grave's disease - TSH receptor autoantibodies mimic TSH and stimulate thyroid gland
* Toxic multinuclear goitre - nodules on thyroid produce thyroid hormone independant of feedback
* Thyroid cancer
* Thyroiditis e.g. De Quervains - first hyperthyroidism then hypo due to negative feedback then return to normal
127
What causes secondary hyperthyroidism (2)
* Pituitary adenoma
* Hypothalamic pathology
128
What are some risk factors for graves disease?(2)
* Family history (gene HLA-DR3)
* Other autoimmune conditions
| These are only really for Graves disease
129
What are some symptoms of hyperthyroidism (4)
* Hot and sweaty
* Weight loss + hyperphagia (being hungary)
* Irritable/ anxious
* Diarrhoea
130
What are some signs of hyperthyroidism (general - 2)
* Tachycardia
* Muscle waisting
131
How is hyperthyroidism investigated
* T4 and TSH plasma levels
* TSH-R auto ABs
* US and UT thyroid/ pit
132
How would T4 and TSH be affected in hyperthyroidism, primary and secondary
* Primary = T4 high, TSH low
* Secondary = T4 high, TSH high
133
How is hyperthyroidism managed (4)
* Adrenergic receptor blockers - e.g. beta blockers, propranolol (non selective)
* Medicines to block thyroid uptake of iodine
* Radioactive iodine - kills thyroid cells, (patient must stay away from kids for few days)
* Surgery
Levothyroxine if patient becomes hypo
| Adrenergic receptor blockers used to treat syptoms as T3 activates SNS
134
What are two medications used for hyperthyroidism
* Carbimazole = 1st line
* Propylthiouracil = 2nd line
135
What are some complications of hyperthyroidism (not gaves complications) (2)
* Thyroid storm = emergency - very high T3/4 levels; fever, high HR
* Osteoporosis
136
How is thyroid storm treated
Same way as hyperthyroidism + supportive treatment e.g. Carbimazole, beta blockers
137
What antibody class causes **G**rave's disease
Ig**G**
138
What is the pathophysiology of Graves
Auto ABs stimulate TSH-R and mimick TSH.
They also affect other body parts such as muscles behind the eyes causing inflammation.
139
What are the symptom unique to Grave's (3)
* Goitre (swollen thyroid)
* Exophthalmos - bulging eyes
* Pretibial myxoedema - buildup of mucin under skin on anterior part of leg
140
What is hypothyroidism (simple)
Lack of thyroid hormones - T3/4
141
What are the two types of hypothyroidism
* Primary - thyroid pathology = less T3/4 independant of TSH
* Secondary - ant. pituitary/ hypothalamic pathology = too little TSH produced/ released *sometimes called hypopituitarism*
142
Who does hypothyroidism mainly affect (2 things)
* Over 40s
* Females (6:1)
143
What causes hypothyroidism (5)
* Hasimoto's thyroiditis
* Iodine deficiency
* Drugs - hyperthyroid drugs, lithium
* Thyroidectomy
* Hypopituitarism - infection, tumour, radiation
144
What is the pathophysiology of Hashimoto's thyroid
AutoABs (e.g. antithyroid peroxidase) attack thyroid gland --> swelling (goitre) --> then atrophy of thyroid
145
What are some risk factors of hypothyroidism
Other AI diseases
146
What are some symptoms of hypothyroidism (5)
* Weight gain
* Fatigue/ lethargy
* Constipation
* Cold intolerance
* Menorrhagia (heavy periods)
147
What are some signs of hypothyroidism (4)
* Bradycardia
* Delayed reflexes
* Goitre
* Oedema
148
How is hypothyroidism investigated and what would the results be
Thyroid function tests
* Primary = low T3/4, high TSH
* Secondary = low T3/4, low TSH
149
How is hypothyroidism treated
Adress underlying cause
then... levothyroxine
150
What is levothyroxine and what happens to it in body
T4 - metabolised to T3
151
What are some complications of hypothyroidism (3)
* Congestive cardiac failure
* Myxoedema coma (hypothermia, difficulty breathing, confusion)
* Pregnancy problems
152
What is hyperparathyroidism
Too high levels of PTH in the blood
153
What are the effects of PTH on Ca2+ (3 things)
* Increase reabsorption of Ca2+ in kidneys
* Increase reabsorption of bone (more osteoclast activity)
* Activate vitamin D3 in kidneys
154
What effects does Vitamin D3 have on Ca2+ (4 things)
* Ca2+ absorption in intestines
* Ca2+ reabsorption in kidneys
* Ca2+ resorption from bone
* Negative feedback on PTH
155
What effect does PTH have on phosphate
* Decreases reabsorption of phosphate in kidneys
*Overall small decrease in phosphate serum levels*
156
Why does a decrease in phosphate mean an increase in Ca2+
Phosphate forms salts with Ca2+, therefore a decrease in phosphate = more ionised calcium circulating
157
Which cells produce PTH
Chief cells in the parathyroid gland
158
What are the three types of hyperparathyroidism
* Primary = Excessive inapropriate production of PTH
* Secondary = hypocalcaemia --> high PTH to compensate
* Tertiary = autonomous production of PTH after resolution of hypocalcaemia due to hyperplasia
159
Main cause of primary hyperparathyroidism
Parathyroid adenoma
160
Causes of secondary hyperparathyroidism (2)
* CKD --> low reabsorption of Ca2+
* Low vit D intake --> decreased absorption of Ca2+ from intestines
161
Cause of tertiary hyperparathyroidism
Prolonged secondary --> hyperplasia of PT gland; unresponsive to -ve feedback
162
What are the signs/ symptoms of hyperparathyroidism (5)
* Renal st**ones**
* Painful b**ones**
* Abdominal gr**oans** - constipation, N+V
* Psychiatric m**oans** - fatigue/ depression
* Polyuria/dipsia = going to toilet more - thr**ones**
163
How is hyperparathyroidism investigated
* PTH/ Ca2+/ phosphate blood tests
* DEXA scan
164
What would PTH, Ca and phosphate be in primary, secondary and tertiary hyperparathyroidism
165
How is hyperparathyroidism managed
* Primary - parathyroidectomy; medication to slow bone loss
* Secondary - calcium correction
* Tertiary - medication to increase calcium sensitivity; parathyroidectomy
166
What medicine is used to slow bone loss in primary hyperparathyroidism
Bisphosphonates
167
What medicine is used to increase calcium sensitivity of the parathyroid gland in hyperparathyroidism
Cinacalcet
168
What is hypoparathyroidism
A lack of plasma PTH
169
What are the types of true hypoparathyroidism
* Primary - pt glands dont produce enough PTH for whatever reason
* Secondary - pt glands dont produce enough PTH due to hypercalcaemia
170
What causes primary hypercalcaemia (3)
* Surgery/ damage/ radiation
* Genetic malformations
* Auoimmune
171
What are the symptoms of hypoparathyroidism (4)
* Convulsions
* Arrhythmias
* Tetany
* Numbness
| CATs go NUMB
172
What are the signs of hypoparathyroidism (2)
* Trosseau's sign - flexion of wrist when BP cuff put on
* Chvostek's sign - spasm of facial muscles when CN7 tapped over parotid gland
| These signs are due to increased firing of nerves due to hypocalcaemia
173
How is hypocalcaemia diagnosed (2)
* PTH low, Ca2+ low, phosphate high
* ECG = long QT syndrome
174
How is hypocalcaemia treated
Treat underlying cause
Give Ad Cal D3 (calcium and vitamin D3 to increase Ca2+ absorption)
175
What is pseudohypoparathyroidism
Lack of responce to PTH at bones and kidneys and can't activate calcidiol
176
What is acromegaly (simple)
Excessive release of GH --> overgrowth of systems
177
What stimulates GH release
Growth hormone releasing hormone
178
What else stimulates GH release
Ghrelin
179
What hormones inhibit growth hormone release (2)
* Somatostatin - major effect
* Dopamine - minor effect
180
What does GH stimulate the release of that also exerts affects throught the body
Insulin like growth factor-1
181
Where is ILGF-1 released from
Liver
182
What are the effects of GH and ILGF-1 (5)
* Increase muscle growth
* Increase bone density
* Increase protein synthesis
* Increase fat/ glycogen breakdown
* Inrcease cell reproduction
183
What causes acromegaly
* Pituitary adenoma
* Lung/ pancreatic GHRH or GH secreting tumour
184
What are the signs/ symptoms of acromegaly (5)
* Changes in body shape/ features
* Bitemporal hemianopia
* Arthritis - growth of joint tissues
* Sleep aponea
* Fatigue
185
What changes in body shape/ features occur in acromegaly
* Large hands/ feet
* Prominent forehead
* Mandibular protrusion
186
What does acromegaly in children cause
Gigantisism
187
How is acromegaly investigated
* ILGF-1 blood test = raised
* OGTT while measuring GH
188
Why is ILGF-1 measured instead of GH for acromegaly diagnosis
ILGF-1 doesn't fluctuate like GH does throught the day
189
How is OGTT used to diagnose acromegaly
Glucose drink given --> GH monitored, should be surpressed by high glucose levels
190
How is acromegaly managed
* Transphenoidal resection surgery
* Medication to inhibit GH
191
What medication is used to treat acromegaly (3)
* Somatostatin analogue (ocreotide)
* Dopamine agonist (bromocriptine)
* GH receptor antagonists (pegvisomant)
192
What are some complications of acromegaly
* T2DM
* Sleep apnoea
* IHD
* Colorectal cancer
193
What is a prolactinoma
Pituitary adenoma that secretes excess prolactin
194
What are the two types of prolactinoma tumours
* micro - less than 10mm on mri
* macro more than 10mm on mri
195
What are the functions of prolactin (2)
* Stimulates lactation
* Breast development
196
What other pituitary hormones does prolactin inhibit
Inhibits GnRH from hypothalamus --> inhibits LH and FSH
197
What are the signs and symptoms of prolactinoma (5)
* Amenorrhea - no periods
* Galactorrhoea - milky discharge
* Gynaecomastia
* Infertility
* Bitemporal hemianopia
198
How is prolactinoma investigated
* Prolactin levels
* MRI
199
How is prolactinoma managed
* Transphenoidal surgery
* Medication
200
What inhibits the production of prolactin
Dopamine
201
What medication is used to treat prolactinoma
Dopamine agonists (bromocriptine) - inhibits prolactin, shrinks tumour
202
What are some complications of prolactinoma (3)
* Sight loss
* Infertility
* Raised ICP
203
What are the two most common and other causes of hypercalcaemia
* Hyperparathyroidism
* Bone malignancies
* Thiazide diuretics, hyperthyroidism, dehydration, high Ca2+ intake
204
What may happen to the ECG trace in those with hypercalcaemia
Short QT segment
205
What are the symptoms of hypercalcaemia (5)
* Psyciatric moans
* Abdominal groans
* Painful boans
* Kidney stones
* Toiletry thrones
206
What are the causes of hypocalcaemia
* CKD (decreases vit d activation) - but can also cause hyper
* Vit D3 deficiency
* Drugs: calcitonin, bisphosphonates (slow bone loss)
207
What is the affect of hypocalcaemia on ECG
Long QT segment
208
What are the symptoms of hypocalcaemia
* Convulsions
* Arhythmias
* Tetany
* Numbness
| CATs go NUMB
209
Hyperkalaemia causes
* Impaired secretion - AKI, CKD, low aldosterone, drugs
* Increased intake
* Shift to extracellular - acidosis, low insulin, sever burns
210
Symptoms/ signs on hyperkalaemia
* Fatigue
* Arrhythmias
* Weakness
* Dyspnoea
211
How is hyperkalaemia investigated
* Bloods: U&Es
* ECG
212
What ECG findings would be present in hyperkalaemia (4)
* No P wave (Go)
* Long PR interval (Go Long)
* Tall T wave (Go Tall)
* Wide QRS complex (Go Wide)
213
How is hyperkalaemia managed (4)
* ABCs
* Calcium gluconate - protects myocardium
* Insulin + dextrose - moves K+ into cells, replaces glucose
* Beta agonist (moves K+ into cells)
214
Hypokalaemia causes
* Increased excretion - CKD, increased aldosterone, D+V, drugs
* Reduced intake
* Shift to intracellular - alkalosis (K+ moves into cells so H+ can move out), drugs e.g. insulin, B2 agonists
215
What are the signs/ symptoms of hypokalaemia
* Arrhythmias
* Fatigue/ weakness
* Hypotonia
* Hyporeflexia
216
How is hypokalaemia investigated
* Blood: U&Es
* ECG
217
How is ECG abnormal in hypokalaemia
* Prolonged PR
* ST depression
* Prominent U wave
* Inverted T wave
218
How is hypokalaemia managed
* IV potassium
* Treat underlying cause
219
How do beta-2 agonists affect K+
Increases activity of Na+/K+ ATPase pump therefore more K+ into cells
| Na/k pump = 3 Na out; 2 K in
