Brainscape's Knowledge GenomeTM

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


See full index

201 cns > endocrine yr3 > Flashcards

endocrine yr3 Flashcards

1
Q

what are the 4 types of hormones

A

1.peptide: insulin, acth, growth hormone, LH,FSH
-protein synthesis
-exocytosis (require stimuli)
-transport: hydrophilic (circulate freely)
2. steroidal: cortisol, aldosterone, sex hormones
-enzymatic conversion of cholesterol
-stimuli increase enzyme activation
-transport: binds with plasma protein
3. tyrosine: thyroid and catecholamines
-pre-cursor: tyrosine
-diffusion across membrane (stimulus)
-binds to plasma protein
4. eicosanoids: prostaglandin, leukotrienes
-peroxidation of arachidonic acid by COX, phospholipase and lipoxygenases
-poorly diffuse
-transport: require a transporter (anionic)

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

what are the targets of peptide and steroid hormones

A

-peptide: GPCR and catalytic receptors (surface)
-steroid: cytosolic and nuclear receptor (inside)

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

what are the causes of hypersecretion and hyposecretion

A

-hypersecretion: tumor (primary or secondary or ectopic), immunological
-hyposecretion: genetic, immunological, destruction by disease (autoimmune disease)

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

what hormones are secreted by anterior and posterior pituitary

A

Anterior: Growth hormone (by somatotropin)
-prolactin (by lactotropon)
-ACTH (by corticotroph)
-TSH (by thyrotrophin)
-LH, FSH (by gonadotropin)
Posterior: oxytocin and ADH

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

what is growth hormone

A

-secreted by acidophilic cells in pituitary
-peptide hormone( 21.4K DA single-chain polypeptide, 190AA with 2 disulphide bridges)
-stored in cells as granules
-increase glucogenesis, increase protein synthesis, increase lipolysis
-increase cell size, cell division and skeletal growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what factors affect levels of GH

A

-blood glucose
-free fatty acid
-sleep
-exercise

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

what are growth hormone disorders

A

Dwarfism: low GH
-can be acquired or congenital
symptoms: low blood sugar, anxiety, osteoporosis, poor muscular tone
treatment: hormone replacement (somatotrpin)
Acromegaly: High GH (hypertension, diabetes, arthritis)
Treatment: surgery, radiation, drugs
Octreotide: slows down GH release (monthly injection)
Pevgisomant: GH receptor antagonist (symptoms)
Bromocriptine: D receptor agonis (stop GH production)

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

what is cortisol (corticosteroid)

A
  • ACTH stimulates adrenal gland to release cortisol
  • steroid hormone
    -increase glucogenesis, protein breakdown and lipolysis
    -anti-inflammatory effect: increase lipocortin which inhibits COX and phospholipase A2 so decrease prostaglandin and thromboxane (also downregulates anti-inflammatory genes)
    -immunosuppressive effect: inhibits humoral factor, suppress immune cell’s maturation, differentiation, proliferation
    -sleep wake cycle: high in the morning, low at night
    -stress response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is Crushing syndrome

A

-high cortisol levels
-obesity, high glucose, high androgen levels, diabetes, depression, sleep disturbances, osteoporosis, susceptibility to infections, CNS irritability
-causes: 80% secondary tumor (pituitary), 10%primary
treatment: secondary-surgery, radiation
primary: metyrapone: CYP11B1 inhibitor
(reduction of conversion 11-deoxycortisol to cortisol)
ketoconazole: CYP17A1 inhibitor
(blocks biosynthesis of cortisol, aldosterone and adrogens)

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

what is Addison disease

A

-not producing adrenal hormones
-autoimmune disease
symptoms: hair loss, blurred vision, abdominal pain, decreased appetite, darkening of skin, hypoglycemia)

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

what are aldosterone disorders

A

-hypoaldosteronism: enzyme deficiency
(hyponatremia, hypovolemia, hyperkalemia)
-conn’s syndrome: hyperaldosteronism
(hypernatremia, hypertension, hypokalemia

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

what does thyroid do?

A

-increases basal metabolic rate
-control metabolism of carbs, fat, proteins
-maintenance of water and electrolyte balance
-regulation of plasma calcium
-work with GH to stimulate bone growth
-maturation of brain during prenatal period
-affects memory, mood, sleepiness, speech
-affects fertility, ovulation and menstruation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how is thyroid produced

A
  • TRH is released from hypothalamus
    -TSH is released from pituitary
    -thyroid follicular cells synthesize thyroglobulin (enters follicular lumen through exocytosis)
    -iodine uptake
    -thyrocytes uptake iodinated thyroglobulin
    -lysosome fuse with endosome containing iodinated thyroglobulin
    -proteolytic enzymes cleave thyroglobulin into MIT, T3, T4
    -T3 and T4 are released into capillaries by MCT8 transporter
    -deionised enzymes remove iodine from MIT and DIT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is thyroid receptor

A

-nuclear TH receptor
-ligand-inducible transcription factor
-two classes (α and β)
-T4 is converted to T3 by D1/D2
-T3 binding to the ligand-binding domain results in movement of carboxyterminal helix 12
-promotes coactivator binding
-recruitment of polymerase III and onset of gene trascription

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

what are the symptoms of hypothyroidism and hyperthyroidism

A

Hypothyroidism: cold intolerance, weight gain, slow heart rate, depression, constipation, muscle pain
Hyperthyroidism: weight loss or gain, increased sweating, anxiety, racing heart, diarrhea, muscle weakness, heat intolerance, increased appetite
both: insomnia and hair loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is thyrotoxicosis and what are the causes

A

-excess thyroid hormone
-increased metabolic rate and appetite
-nervousness, sweaty, tachycardia, tremor, wide stare
Causes:
Hyperthyroidism: grave’s disease (autoimmune)
goiter, iodine-induced hyperthyroidism, pituitary tumor
Thyrotoxicosis: autoimmune thyroiditis or drug-induced thyroiditis (amiodarone, lithium, interferon, tyrosine kinase inhibitors)
-exogenous thyroid hormone

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

what is the treatment of hyperthyroidism

A

-oral carbimazole, methimazole, propylthiouracil
(inhibition of iodide oxidation, inhibition of iodination of tyrosine, inhibition of coupling of iodotyrosines)
-iodides
-b-blockers: propanolol or atenolol (symptom relief)

18
Q

what is a thyroid storm and how is it managed?

A

-large amounts of thyroid suddenly (infection or surgery)
-palpitations, tachycardia, tremor, vomiting, seizures, confusion
-treatment: potassium iodide, carbimazole, rehydration, B-blockers steroids

19
Q

what causes hypothyroidism and how is it managed?

A

causes: autoimmune thyroiditis (Hashimoto’s disease)
congenital dysfunction, iodine deficiency, thyrotoxycosis
Treatment: replacement (levothyroxine sodium)

20
Q

what is osteoporosis and what is the pathophysiology

A

-low bone mass
-abnormal bone architecture
-reduced bone streght
T-score< -2.5 (bone mineral density)
-imbalance in bone remodeling and formation by osteoclasts and osteoblasts

21
Q

what are the risk factors of osteoporosis

A

-endocrine disease
-GI conditions
-chronic diseases
-menopause
-immobility
-age
drugs( oral corticosteroids, PPIs, SSRIs, carbamazepine, heparin, methotrexate, antiretrovirals)
-alcohol
-rheumatoid arthritis

22
Q

how to assess osteoporosis

A

-Qfracture risk:
High risk (>10%): offer drugs treatment and DEXA
Intermidiate: DEXA for BMD measurment
Low risk: lifestyle advice (healthy diet, calcium intake, VitD, exercise, smocking, less alcohol, low BMI)

23
Q

what is the drug treatment of osteoporosis

A

-Bisphosphonates: inhibit bone resorption (increase BMD)
-denosumab: inhibit osteoclasts (6 month injection)
*calcium levels corrected first
-Teriparatide: menopausal women, high risk men or corticosteroid-induced osteoporosis
-romosozumab: inhibit sclerosin, decreases resorption
*CVD effects, stroke, hypocalcaemia (caution)
- Raloxifene: selective oestrogen receptor modulator

24
Q

when should steroids be withdrawn gradually

A

-receive more than 40mg prednisolone daily for more than 1 week
-been given repeat doses in the evening
-received more than 3 week treatment
-recently taken repeated doses (more than 3 weeks)
-taken a short course within a year after stopping long term course
-other possible causes of adrenal suppression

25
Q

when should you give steroid emergency cards

A

-primary adrenal insufficiency
-adrenal insufficiency due to hypopituitarism requiring corticosteroid replacement
-doses equivalent to or exceeding prednisolone 5mg OD for 4 weeks or longer across all administration routes
-received more than 40mg prednisolone for more than 1 week or repeated short courses
-taken a short course within a year of stopping long term treatment

26
Q

what are the contraindications of HRT

A

-current or past breast cancer
-known or suspected estrogen-dependent cancer
-undiagnosed vaginal bleeding
-untreated endometrial hyperplasia
-previous or current VTE
-angina or MI
-liver disease
-pregnancy

27
Q

what are the pharmacokinetics of metformin

A

-Absorption: 20% in duodenum, 60% in jejunum and iluem
organic cation transporter OCT1, oral bioavailability:40-60%
-distribution: no binding, hepatic uptake by OCT1 and 3
-no metabolism
-excretion: renal excretion mediated by OCT-2

28
Q

what factors affect high clearance of metformin

A

-low molecular weigh
-negligible plasma protein binding
-presence of transporters in kidney
-low lipid solubility which makes negligible passive reabsorption

29
Q

what are the pharmacokinetics of pioglitazone

A

-absorption: completely in GI
-distribution: plasma, liver and kidney, protein binding
-metabolism: by CYP2C8 and CYP3A4 (3 active metabolites)
-excretion: 64% in urine and bile

30
Q

what are the pharmacokinetics of sulfonylureas

A

-well absorption (2-4 hr concertation peak)
-bound to plasma proteins
-metabolism: liver
-excretion: urine

31
Q

what are the pharmacokinetics of meglitinides

A

-well absorbed, 56% bioavailability
-metabolism: liver (CYP450 2C8 and 3A4
-excretion: 90% in stool

32
Q

what affects oral peptide delivery

A

-pH in stomach
-enzymatic degradation in GI tract
-intestinal mucus layer
-influence of bile
-GI transit time

33
Q

what is the structure of liraglutide

A

-GLP-1 analogue
-Lys34 replaced by arginine (resistance to DPP
-c16 acyl chain attached to Lys26 via a glutamoyl spacer
-affinity for serum albumin

34
Q

what is the structure of semaglutide

A

-amino acids at position 8 and 34 replaced by α-aminobutyric acid and arginine (resistance to DPP-IV)
-Lys26 is acylated with stearic diacid
(affinity for albumin and resistance to DPP-IV)

35
Q

what is oral semaglutide

A

-with an absorption enhancer SNAC-300mg (salcaprozate sodium)
-increase peptide hydrophobicity
-SNAC neutralizes pH preventing pepsin activation
-semaglutide released as multimers (protect from enzymes)
-SNAC causes monomers of peptide to be formed
-SNAC inserts in plasma membrane of gastric epithelium and perturbs it via fluidization without directly opening tight junctions
-semaglutide fluxes across the epithelium by transcellular route

36
Q

what are the strategies for improving oral peptides

A

-peptide in nanoparticle
-peptidase inhibitor
-permeation enhancer

37
Q

what are the components of oral insulin
how does POD technology work

A

-EDTA: cacium-chelating, opening and membrane perturbation
-bile salts and omega 3 fatty acids (detergent surfactanct action)
-peptidase inhibitors

38
Q

how does CAPIC work

A

-aggregating casein around around a formulation of PEG and insulin
*casein: protect insulin in GI tract and allows the drug to remain concentrated at site of absorption
-calcium phosphate: helps in reducing acid-induced degradation

39
Q

what are the pharmacokinetics of SGLT-2 inhibitors

A

-oral bioavailability; 78%
-protein bound (91%)
metabolism: primary liver, kidney
excretiom: 72% in urine

40
Q

what are the pharmacokinetics of acarbose

A

-poorly absorbed (35%)
-metabolised by intestinal bacteria
-excreting in urine and stool

201 cns (9 decks)

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