PP Clues 1 Flashcards
(50 cards)
CCK:
- Made by
- Stimulus
- Inhibition
- Where it goes
- What it does
- 2nd messenger
- Misc syndromes
Made by: I cells in duodenum
Stimulus: food (especially fats)
Inhibition: incr pH (alkalosis)
Where it goes: pancreas (digestive enzyme) + gallbladder (bile)
Function: fat + protein digestion
2nd messenger: IP3/DAG
Misc: reason for RUQ pain in gallbladder disease after fatty meal; decr CCK release; if TPN: incr risk of gallstones
Secretin:
- Made by
- Stimulus
- Inhibition
- Where it goes
- What it does
- 2nd messenger
Made by: S cells in duodenum
Stimulus: decr pH
Inhibition: incr pH
Where it goes: Paracrine = duodenum
Function: stimulates production of bicarb from pancreas and inhibits gastrin + gastric motility
2nd messenger: cAMP
What pancreatic hormone has no known function?
Pancreatic polypeptide
From F cells
Hormone that inhibits peristalsis and hunger
Secreted where?
Leptin
Secreted by stomach and adipose
Hormone that promotes hunger and food intake
Secreted where?
Ghrelin
GHRRR when you’re hungry
Gastrin:
- Made by
- Stimulus
- Inhibitor
- Where it goes
- What it does
- 2nd messenger
- Misc syndrome
Made by: antrum of stomach
Stimulus: incr pH
Inhibitor: decr pH
Where it goes: parietal cells of the stomach (mostly body)
Function: production of HCl and intrinsic factor
2nd messenger: calcium
Misc: gastrinoma, incr gastrin; ulcers all the way down ileum
Glucagon:
- Made by
- Stimulus
- Inhibitor
- Where it goes
- What it does
- 2nd messenger
- Misc syndrome
Made by: alpha cells of pancreas
Stimulus: hypoglycemia, stress
Inhibition: hyperglycemia
Where it goes:
- adrenal cortex for Gluconeogenesis
- liver for Gluconeogenesis and ketogenesis
- adipose tissue for lipolysis
Function: gluconeogenesis, Glycogenolysis, ketogenesis, lipolysis
2nd messenger: cAMP
Misc: glucagonoma (incr glucose, incr lipids, incr ketones)
Timeline of stress hormones
- immediately
- 20 minutes
- 2–4 hours
- >24 hours
Immediately: epinephrine
- stimulates glycolysis, Glycogenolysis, gluconeogenesis
20 min: glucagon
2–4 hours: cortisol
- incr glucose by protein breakdown
> 24 hours: growth hormone
- incr glucose by proteolysis
Places that store glycogen(s)
1) skeletal muscle
2) liver
3) adrenal cortex
4) heart
5) intestine wall
Dx if increased levels of VMA, HVA, or metanephrines
OR
BP drops quickly after phentolamine
Pheochromocytoma or neuroblastoma
VMA -> breakdown of Epi
HVA -> breakdown of dopamine
Metanephrines -> breakdown of norepinephrine
Phentolamine is a short-acting alpha blocker
Dx of dancing feet and dancing eyes in a child
Neuroblastoma
Dancing feet -> hypsarrhythmia
Dancing eyes -> opsoclonus
Most common abdominal mass in children
Dx of intermittent palpitations, HTN, diaphoresis, and HA
An excess of NE and Epi causes sympathetic overdrive
- Pheochromocytoma
- Neuroblastoma
-> hypsarrhythmia (dancing feet)
-> opsoclonus (dancing eyes)
-> most common abdominal mass in children
Epinephrine:
- Made by
- Stimulus
- Inhibitor
- Where it goes
- What it does
- 2nd messenger
Made by: adrenal medulla
Stimulus: ACh, stress or hypoglycemia
Inhibitor: hyperglycemia
Where it goes: liver and adrenal cortex
(Only places w/ glucose-6-phosphatase)
Function: gluconeogenesis and Glycogenolysis
2nd messenger: cAMP
2 organs that conduct gluconeogenesis
Liver
Adrenal cortex
(Only places that have the enzyme glucose-6-phosphatase)
MOA of Flutamide
Blocks DHT receptors
- treatment of prostate cancer only
MOA of Finasteride
Blocks 5-alpha reductase
Management of increased cortisol:
- low dose dexamethosone
-> suppression?
-> no suppression?
-> incr ACTH?
-> decr ACTH?
Low dose = 0.5 mg IV Q6x4
-> suppression: physiologically normal
-> no suppression: Cushing’s
-> incr ACTH: small cell lung cancer or pituitary adenoma
-> decr ACTH: adrenal adenoma
Management of incr cortisol:
- high dose Dexamethasone
-> suppression?
-> no suppression?
High dose = 1 mg IV Q6x4
-> suppression: pituitary adenoma
-> no suppression: small cell lung cancer
Bone Terminology:
- incr scarring
Osteosclerosis
Bone Terminology:
- Inflammation of bone causing scarring
Osteitis fibrosis cystica
Bone Terminology:
- incr osteoclastic activity w/ incr alkaline phosphatase
Osteitis deformans
(Paget’s disease)
Bone Terminology:
- decr osteoclastic activity which obliterates bone marrow
Osteoporosis
Dx of DEXA scan with T-score >-2.5
Osteopenia
- decr bone density could be matrix or mineralization
- combo of osteoporosis and osteomalacia
Dx of:
- decr bone density
- decr bone matrix
- DEXA scan with T-score <-2.5
Osteoporosis
- in menopause: decr estrogen -> loss of osteoclastic inhibition, loss of matrix
Treatment:
- 1st = bisphosphonates
- 2nd = raloxifen or teriparatide