Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

FOP/TAS > Endocrine > Flashcards

Endocrine Flashcards

1
Q

describe the posterior pituitary gland production of hormones

A
  1. hypothalamus
  2. posterior pituitary gland
  3. produce oxytocin -> causes uterus contraction and expresses milk
  4. produces ADH which acts at V2 receptors in collecting ducts to increase water reabsorption and V1 receptors on blood vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

which hormones does the anterior pituitary gland produce

A
  1. GnRh -> LH and FSH
  2. TRH -> TSH
  3. PRH -> prolactin
  4. GHRH -> growth hormone
  5. CRH -> ACTH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

describe the action of ACTH

A
  1. hypothalamus stimulated
  2. corticotropin relasing hormone release
  3. acts at anterior pituitary gland to release ACTH
  4. acts at adrenal cortex by binding to melanocortin 2 receptors and stimulates zona fasciculata to produce cortisol and zone reticularis to produce androgens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

regions of adrenal cortex and actions

A
  1. zona fasciculata -> produce cortisol and glucocorticoids
  2. zona reticularis -> produce androgens
  3. zona glomerulosa -> produce mineralocorticoids (aldosterone) - controlled by renin angiotensin system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

describe growth hormone release

A
  1. hypothalamus stimulated and release growth hormone releasing hormone
  2. acts at anterior pituitray gland and produces growth hormone
  3. growth hormone acts at liver and stimulates insulin growth factor 1
  4. causes lipolysis, glycogenolysis , protein synthesis, muscle strength, skeletal growth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

action of LH

A

TESTES -> stimulates leydig cells and produces testosterone

OVARIES -> binds to theca cells + follicular cells to cause steroidgenesis + produce oestrogen

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

action of FSH

A

TESTES -> drives sperm production in sertoli cells and synthesis of androgen binding proteins

OVARY -> binds to granulosa cells to stimulate follicle growth, convert androgens to oestrogen and progesterone production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

risk factors for type 1 diabetes

A
  • family history - twins 30-50% risk of other twin developing diabetes
  • genetics - DR3, DR4, DQA, DQB
  • viral trigger
  • autoimmune conditions
  • cystic fibrosis
  • down syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

embryology of pancreas

A

develops week 5
2 outpouchings develops from ENDODERM lining of duodenum :
1. ventral bud -> lower part of head
2. dorsal bud - upper part of head, neck and tail

from week 7, secretion of hromones
week 10, alpha cells diefferentiate first, then delta and beta
week 15, glucagon detected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

cells of islets of langerhans in pancreas

A

alpha cells - produce glucagon (promotes gluconegogenesis in liver)
beta cells - produces insulin
delta cells - produce somatostatin

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

action of insulin

A

increase glucose uptake into adipose tissue and muscle (via gLUT4 receptor) + suppresses hepatic glucose release and stimulates glycogen synthesis

insulin release from beta cells when blood sugar high and detected by ATP sensitive k channel

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

pathophysiology of type 1 diabetes

A
  1. immune mediated destruction of beta cells via CD4 T lymphocytes (glutamic acid decarboxylase antibdoies, insulin antibodies, islet autoantigen 2)
  2. once 80-90% beta cells destroyed, symptoms develop and deficiency of insulin
  3. increase in counter regulatory hormones (cortisol, adrenaline, growth hormone) and promotes gluconeogenesis, glycogenolysis and ketogenesis in liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

presentation of type 1 diabetes

A

DKA !!
polyuria - caused by overloading of SGLT2 receptors in PCT
polydipsia
weight loss
tiredness
increased skin infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

diagnosis of type 1 diabetes

A

random glucose >11.1mmol
fasting blood sugar > 7.0 mmol/l

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

investigations to do in type 1 diabetes

A
  1. coeliac and TFT markers
  2. HbA1c - average blood sugar over 8 weeks
  3. antibody markers e.g. GAD, islet cells, insulin
  4. U&E
  5. c peptide - indicates T2DM
  6. triglycerides - low HDL, elevated triglycerides
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

target blood sugars

A

waking and before meals: 4-7
after meals: 5-9

for hypoglycaemia - give 10 g oral sugar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

types of insulin therapy

A
  1. basal bolus regime
    - long acting insulin (40% daily dose)
    - short acting insulin with carb counting (60% daily dose - 20% each meal)
  2. continuous insulin pump
    regular amount of rapid acting insulin, resisted every 2-3 days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

annual screening in diabetes

A

blood pressure
urine dipstick - early morning urine albumin : creatinine ratio
eye screen
autoimmune disease screen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the somogyi effect

A

well controlled with night time hypoglycaemia and early morning glycosuria

common with fast acting insulins and managed by reducing insulin dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

indicators of type 2 diabetes

A

obesity **
strong family histroy
acanthosis nigricans (dry, dark patches of skin in axilla or groin)
PCOS
strong FH

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

pathology of T2DM

A

insulin resistance + reduced insulin secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

management of t2DM

A

weight loss and exercise
metformin (suppresses hepatic glucenognesissi)
+/- sulfonylureas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

cause of maturity onset related diabetes mellitus

A

genetic defect in HNF gene (glucokinase receptor = glucokinase deficiency) in beta cells
autosomal dominant
causes asymptomatic, non obese with mildly raised chronic blood sugars

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

screening for MODY

A

urine c peptide creatinine ratio
and genetic testing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

causes of hypoglycaemia

A

ENDOCRINE
hyperinsulinism, growth hormone deficiency, hypothyroidism

METABOLIC
fatty acid oxidation disorders, glycogen storage disorders

NEONATAL
hypothermia, maternal meds / GDM, prematurity, polycythaemia, beckwith wiedeman

OTHER
sepsis, malabsorption, diabetes, liver failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

define gluconeogenesis

A

generation of glucose from non carbohydrate substrates e.g. pyruvate, lactate, glycerol in the liver

occurs during time of fasting/ starvation/ exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

define glycogenolysis

A

breakdown of glycogen in the hepatocytes to produce glucose for cell utilisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

presentation of hypoglycaemia

A

autonomic - tremor, pallor, tachycardia, sweating
behavioural - irritable, hungry, tantrums
neurological - headache fatigue, lethargy, comas, seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

hypoglycaemia screen

A
  1. blood glucose
  2. blood ketones - if low/normal = fatty acid oxidation probelm or ketogenesis problem
  3. insulin and c peptide levels - should be suppressed, high = hyperinsulinaemia
  4. lactate - increased in glycogen storage disorder
  5. free fatty acids
  6. ammonia - elevated in inborn errors of metabolism
  7. acylcarnitines - abnormal in fatty acid defects
  8. urinary organic acids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

pathophysiology of DKA

A
  1. deficiency of insulin
  2. increase in counter regulatory hormones
  3. increase production of glucose from liver thoygh glycogenolysis and gluconeogenesis
  4. free fatty acids converted to ketones by glucagon (acetoacetic acid and beta hydroxybutyric acid)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

presentation of DKA

A

vomiting, abdo pain
dehydration
fever
kussmauls bretahing
shcok
drowsiness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

severity of DKA

A

mild: ph 7.2-7.29 (5% dehydration)
moderate: ph 7.1 - 7.19 (7% dehydration)
severe: ph < 7.1 +/- bicarb <5 (10% dehydration)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

management of DKA

A
  1. ABCDE
  2. IV fluids: 10ml/kg iV fluid bolus of 0.9% saline over 60 minutes (20ml/kg if shocked)
  3. iV fluids: deficit (over 48 hours) + maintenance (24hrs)
  4. insulin therapy 0.1units/kg/hr continuous pump (start 1-2 hours after fluid)
  5. blood glucose and ketones checked 1-2 hourly + gas and U&E every 4 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

complication of DKA and management

A

CEREBRAL OEDEMA - within 12 hours

treat with 20% mannitol 1g/kg over 10-15 minutes or 3% hypertonic saline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

risk factors for developing cerebral oedema in DKA

A

younger age
low pCO2
>40ml/kg fluid bolus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

circulation of thyroid hormones

A

70% of T4 and 50% of T3 bound to thyroxine bidning globulin in circulation

0.03% T4 nad 0.3% T3 unbound in circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

causes of congenital hypothryoidism

A
  1. ectopic gland - most common cause in developed countries
  2. iodine deficiency - most common cause worldwide
  3. dyshormongenesis - consanguinous marriages
  4. thyroid dysgenesis - fails to develop
  5. Hashimotos
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

describe hashimotos disease

A

painelss goitre and hypothyroidism
high anti thyroglobulin antibodies + high anti thyroid microsomal antibodies + high TPO antibodies **

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

detection of congenital hypothyroid

A

NEWBORN SCREENING - TSH measured day 5 of life

if >10 -> USS and isotrope scanning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

presentation of neonatal hypothyroid

A

symptoms around 6 weeks old
poor feeding
prolonged jaundice
hypotonia
constipation
myxoedema - macroglossia, coarse facie, swollen eyelids
cold mottled skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

causes of acquired hypothyroidism

A

Hashimotos
autoimmune thyroiditis
post thyroid surgery
radiation
iodine deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

describe thyroglossal cyst

A

midline neck cyst
moves on tongue protrusion

USS and surgical excision

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

blood results for hypothyroidism

A

low T4, raised TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

blood results for poor compliance with hypothyroidism

A

normal T4, high TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

embryology of parathryoid gland

A

originates from 3rd and 4th branchial arches

46
Q

blood test of hypoparathyroid

A

low PTH
low Calcium
raised phosphate

47
Q

causes of hypoparathyroidism

A
  1. Di george syndrome
  2. removal of thyroid gland affecting parathyroid
  3. Mg deficiency
  4. autoimmune disease
  5. pseudohypoparathyroidism
48
Q

blood tests for pseudohypoparathyroidism

A

high PTH
low Ca
high phosphate

49
Q

signs of hypercalcaemia

A

paraesthesia
cramps
tetany - Chvoseks sign
diarrhoea
carpal spasm - Trousseus sign
ECG - short QT, VF, Osborn waves

50
Q

causes of hypercalcaemia

A
  1. TB
  2. sarcoidosis
  3. FH of MEN1
  4. vit D therapy
  5. williams syndrome
  6. bone mets, myeloma
  7. paraneoplastic syndrome
51
Q

cause of hyperthyroidism

A

Graves disease ***
thyroid carcinoma

52
Q

blood tests in Graves disease

A

raised T3 and raised T4
low TSH
thryoid stimulating hormone receptor antibody

53
Q

management of graves disease

A
  1. carbimazole
  2. propranolol and iodine solution if severely throtoxicsosi
  3. radioiodine and surgery
54
Q

inheritance of CAH

A

autosomal recessive

55
Q

most common cause of CAH

A

21 hydroxylase deficiency in 90% of cases on chromosome 6

causes :
1. accumulation of 17-alpha- hydroxyporgesterone which can be converted to androgens
2. reduced aldosterone production

56
Q

how do girls with CAH present at newborn

A

virilisation and ambiguous genitalia

57
Q

how do boys with CAH present

A

in first week of life with ‘adrenal crisis’ / ‘salt losing crisis’

hypotension
vomiting
dehydration
poor feeding
virilisation in boys

58
Q

blood results of ‘salt losing crisis’ in CAH

A

hyperkalaemia
hyponatraemia
hypoglycaemia
metabolic acidosis

59
Q

how to test for CAH

A
  1. karyotype*
  2. 17 hydroxyprogesterone raised* - need to be at least 72 hours old
  3. pelvic USS
  4. 11-doxycortisol reduced
60
Q

management of CAH

A
  1. hydrocortisone
  2. fludrocortisone
  3. sodium replacement in 1st year of life

IN SALT LOSING CRISIS:
1. IV 10% dextrose 3ml/kg
2. iV hydrocortisone 60mg/m2
3. IVF with O.9% saline

61
Q

cause of cushings syndrome

A
  1. iatrogenic steroids
  2. pituitary tumour secreting excess ACTH
  3. adrenal adenomas or carcinomas
  4. MEN1
  5. mccune albright syndrome
62
Q

presentation of cushings syndrome

A
  1. central weight gain, risk of diabetes, moon face (due to insulin resistance and increased blood sugar)
  2. increased infections (immunosupressed)
  3. muscle weakness
  4. easy bruising, striae (impacts collagen synthesis)
  5. hypertension, risk fo CV disease
  6. depressed, irritable, mood variable
63
Q

investigations for cushings syndrome

A
  1. 24 hour urinary free cortisol levels high ** - loss of diurnal variation of cortisol
  2. serum ACTH levels
  3. IPSS *
  4. dexamethasone suppression test
  5. MRI head !
64
Q

management of cushings

A

surgical intervention for tumours
metyrapone - lowers cortisol level

65
Q

blood results of long term steroid use

A
  1. low cortisol
  2. low ACTH
  3. low CRH

causes suppression of the HPA and reduced synthesis of CRH and ACTH and downregulation of natural glucocorticoid

need to manage infectiosn with double dose steroids

66
Q

describe GH deficiency

A

inadequate production or secretion of growth hormone by anterior pituitary gland

can be idiopathic, genetic, acquired through trauma/ radiation

67
Q

presentation of GH deficiency

A

short stature - present early or mid childhood
delayed skeletal maturation - bone age younger than chronological age
reduced muscle bul and increased s/c fat
isolated

68
Q

describe diabetes insipidus

A

insufficient ADH causing high volumes of dilute urine and hypernatraemia dehydration

69
Q

central/ cranial causes of diabetes insipidus

A

= DEFICIENCY OF ADH DUE TO REDUCECD SECRETION BY HYPOTHALAMUS

trauma
post radiotherapy
infections
craniopharyngioma - following neurosurgery
hypothalamic glioma
familial AD neurohypophydeal DI

70
Q

nephrogenic causes of diabetes insipidus

A

= RESISTANT TO ADP IN KIDNEYS

renal damage e.g. CD
nephrotoxic medications e.g. lithium
hypokalaemia, hypercalcaemia
hyperglycaemia induced osmotic diuresis

71
Q

Presentation of diabetes insipidus

A

polyuria
dehydration
polydipsia

72
Q

diagnostic tests for diabetes insipidus

A
  1. paired urine and serum osmolalities
    dilute urine (osmolality <750) + hyperosmolar state (>295)
  2. MRI brain
  3. water deprivation test - once given desmopressin dose, if get a rise in urine = cranial DI / if no rise in urine osmolality = nephrogenic DI
73
Q

management of central diabetes insipidus

A

desmopressin

74
Q

management of nephrogenic diabetes insipidus

A

thiazide diuretics (inhibit NaCl cotransporter in the DCT and increase proximal tubular Na and water reabsorption)

75
Q

describe SIADH

A

excessive secretion of ADH causing water retention and leading to dilutional hyponatraemia

76
Q

causes of SIADH

A
  1. tumours - small cell lung cancer, brain tumours, thyoma, Ewings sacroma
  2. CNS - trauma, infection, haemorrhage
  3. medications - thiazide diuretics, SSRI, anti epileptics
  4. TB
77
Q

presentation of SIADH

A

headache
confusion
lethargy
N&V
hyponatraemia - muscle cramps

78
Q

diagnostic tests for SIADH

A
  1. serum osmolality - low
  2. urine osmolality - high (concentrated urine)
  3. hyponatraemia
79
Q

management of SIADH

A
  1. fluid restriction
  2. monitoring electrolytes
  3. vasopressin receptor antagonists e.g. tolvaptan
80
Q

describe phaeochromocytomas

A

neuroendocrine chromaffin cell tumour which commonly occurs in the adrenal medulla

associated with NF1

81
Q

Presentation of phaeochromocytomas

A

headache
sweating
palpitations
diarrhoea
severe hypertension

82
Q

diagnostic test for phaeochromocytomas

A

urine catecholaemines metabolites

83
Q

management of phaeochromocytomas

A
  1. alpha adrenoreceptor blockade
  2. surgical excision
84
Q

inheritance of MEN type 2b

A

autosomal dominant - mutation in RET proto oncogene

85
Q

presentation of MEN type 2b

A
  1. mucosal neuroma
  2. medullary thryoid cancer
  3. pituitary tumour
  4. parathyroid hyperplasia -> hyperparaparathyroidism
86
Q

inheritance of kallmann syndrome

A

X linked recessive
isolated deficiency of GnRH -> causes hypogonadism, infertility and incomplete/ absent puberty

87
Q

presentation of kallman syndrome

A

hypogonadotropic hypogonadim
obesity
anosmia
colour blind

88
Q

normal puberty ages

A

8-14 y/o in girls
9 - 14 y/o in boys

89
Q

normal puberty patten in girls

A

1st sign = breast development (breast buds appear at age 11 in 50%)
2. pubic and axillary hair growth
3. menarche 2-3 years after breast bud development
4. peak height velocity

90
Q

normal puberty pattern in boys

A

1st sign= testicular enlargement to > 4mls (usually 12- 13 y/o)
2. pubic hair growth 1-2 years after
3. penile and scrotal enlargement one year after testicular enlargement
4. later signs = growth spurt (once testicular growth >10mls) deep voice, acne, facial hair

91
Q

define precocious puberty

A

secondary sexual characteristics (breast bud enlargement and testicular enlargement) develop before age of 8 in GIRLS and before of 9 in BOYS

92
Q

2 type of precocious puberty

A
  1. true central precocious puberty (80%)
    = gonadotropin dependent = premature stimulation of HPA axis, causes same physiological pattern of puberty
  2. androgen mediated precocious puberty (20%)
    = gonadotropin independent= early excess andogen secretions, causes virilisation
93
Q

causes of true central precocious puberty

A
  1. idiopathic - girls (80%), premature physiological puberty
  2. CNS abnormalities - NF1, septo optic dysplasia ,tumours, hydrocephalus
  3. leydig cell tumours (secrete testosterone)
94
Q

causes of androgen mediated precocious puberty

A
  1. adrenal disorders - CAH, severe hypothyrodisim, adrenal tumours
  2. russel silver syndrome
  3. mccune albright syndrome

causes secondary sexual characteristics with pre pubertal testes

95
Q

features of mccune albright syndrome

A

fibrous dysplasia
cafe au lait macules
endocrine hyperfunction - thyrotoxicosis, cushings
early puberty

mutation in gNAS-1

96
Q

investigations for precocious puberty

A
  1. gonadotropin levels - differentiates between central and androgen related causes
    central = high FSH and high LH and high sex steroids
    androgen = low FSH and low LH
  2. androgen levels (testosterone and oestrogen)
  3. pelvic USS
  4. hand and wrist X R to assess bone age
97
Q

management of precocious puberty

A

central = gonadotropin releasing hormone anologues to suppress gonadoptropins

androgen = GnRH anologues

98
Q

describe delayed puberty

A

onset of sexual development later than 13 y/o in girls and 14 y/o in boys

99
Q

causes of delayed puberty

A
  1. constitutional delay ***
  2. chronic illness e.g. anorexia, CD, post chemo, coeliac, hypothyroid
  3. malnutrition
  4. genetic - klinefelters, Kallmann syndrome, turners, prader willi syndrome
  5. chronic steroid use
  6. hypogonadotropic hypogonadism - low FSH, LOW FH and low testosterone. reduced GnRH
100
Q

investigations for delayed puberty

A
  1. LH and FHS
  2. Testosterone and oestradiol
  3. prolactin + TFT
  4. karyotype
  5. bone age
101
Q

how to calculate mid parental height

A

(dads height + mums height)/2
+7cm for boys
-7cm for girls

plot on growth chart for 18 y/o
shoudl be within 2 centile spaces

102
Q

causes for tall stature

A
  1. constituitional tall stature - tall parents, normal growth velocity, have advanced bone age
  2. genetics - marfans, klinefelters, sotos (lareg head and obesity), beckwith wiedeman
  3. endocrine - hyperthryroid, growth hormone excess, CAH, precocious puberty
  4. homocystinuria
103
Q

causes of short stature

A
  1. constitutional delay of growth - had deceleration of height in 1st 3 years, normal in child and accelerated in adolescent
  2. familial short stature
  3. primary growth disorder e.g. downs, prader willi, turner, noonan, achrondoplasia
  4. endocrine - hypothyroid, hypopituitarism, Cushings, glycogen storage disorders, growth hormone deficiency
  5. malnutrition, neglect, psychosocial deprivation
  6. chronic disease e.g. CKD, CHD, coeliac
104
Q

investigations for short stature

A
  1. mid parental height
  2. bone age *
  3. karyotype
  4. TFT, coeliac, FBC
  5. serum IGF1 and IGFBP3 - better levels than GH (variation in day)

weight: if high -> GH deficiency, hypothyroid
proportionate height and weight -> genetic testing

105
Q

side effects of carbimazole

A

cholestatic liver injury -> itching
nausea, vomiting, diarrhoea
thinning of hair
agranulocytosis

106
Q

which hormone stops growth

A

oestrogen -terminates growth by causing fusion of epiphysis at long bones

106
Q

mechanism of action of sulfonylureas

A

act at ATP sensitive K channel in beta cells and increases release of insulin

SE = hypoglycaemia, weight gain

106
Q

ECG in hyperkalaemia

A

tall tented T waves
PR prolonged

106
Q

bloods for central hypothyroidism

A

reduced TSH
reduced T3/T4

106
Q

Define congenital hypopituitarism

A

deficiency of GH + at least one other anterior pituitary hormone

microgenitalia, jaundice, hypoglycaemia, jittery

107
Q

role of leptin

A

reduces food intake and appetite - produced in adipose cells and acts on hypothalamus

108
Q

features of sotos syndrome

A

large since birth
tall
macrocephaly
long narrow face and pointed chin
down slanting palpebral fissures
developmental delay and LD
protrduing forehead

FOP/TAS (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions