PP Clues 1 Flashcards
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
ANP:
- Made by
- Stimulus
- Inhibition
- Where it goes
- What it does
- 2nd messenger
Made by: right atrium, right ventricle, brain
Stimulus: incr volume
Inhibitor: decr volume
Where it goes: kidney
Function: dilates afferent renal artery, inhibits aldosterone
2nd messenger: NO (broken down by neprilysin)
(BNP is brain version and made in right ventricle)
Somatostatin:
- Made by
- Stimulus
- Inhibitor
- Where it goes
- What it does
- 2nd messenger
- Misc syndrome
Made by: D cells in the duodenum; delta cells in pancreas
Stimulus: duodenal hormones
Inhibition: incr pH
Where it goes: Paracrine (duodenum)
Function: purely inhibitory
2nd messenger: cAMP
Misc: somatostatinoma -> can occur alone as part of MEN1; severe constipation
VIP:
- Made by
- Stimulus
- Inhibition
- Where it goes
- What it does
- 2nd messenger
- Misc syndrome
Made by: Auerbach plexus in the duodenum
Stimulus: duodenal hormones
Inhibition: incr pH
Where it goes: Paracrine (duodenum)
Function: purely inhibitory
2nd messenger: cAMP
Misc: VIPoma -> usually pancreatic tumor -> watery secretory diarrhea
GIP:
- Made by
- Stimulus
- Inhibition
- Where it goes
- What it does
- 2nd messenger
- Misc syndrome
Made by: G cells in duodenum
Stimulus: glucose
Inhibitor: incr pH
Where it goes: pancreatic islet cells
Function: enhances insulin secretion, inhibits glucagon secretion
2nd messenger: cGMP
Misc: dumping syndrome -> seen after gastric bypass causes osmotic diarrhea leads to DM T2
Motilin:
- Made by
- Stimulus
- Inhibition
- Where it goes
- What it does
- 2nd messenger
Made in: duodenum
Stimulus: decr pH or small bowel distention
Inhibition: incr pH
Where it goes: Paracrine (duodenum)
Function:
- peristalsis, specifically segmentation
- controls secondary peristalsis (= migrating myenteric complex = MMC)
2nd messenger:
- IP3/DAG during meals
- Ca/Calmodulin between meals
Decr response to edrophonium
Edrophonium MOA: AChE inhibitor
Decr response: Lambert-Eaton
Incr response to edrophonium
Edrophonium MOA: AChE inhibitor
Incr response: myasthenia gravis
Where does CMV remain latent?
Macrophages
- most commonly picked up in blood transfusions and organ transplants
Where does EBV remain latent?
B cells
Dx of necrotizing glomuleronephritis
Wegener’s
Granulomatosis w/ polyangiitis
Anti-proteinase 3 = c-ANCA
Incr bleeding time
No change in platelets
Dx of positive anti-proteinase 3 (anti-PR3)
Wegener’s
Granulomatosis w/ polyangiitis
Anti-proteinase 3 = c-ANCA
Dx of positive anti-myeloperoxidase (anti-MPO)
Churg-Strauss
Eosinophilic granulomatosis w/ polyangiitis
Anti-MPO = p-ANCA
Bacteria causing bloody diarrhea (3)
Shigella (inflammatory)
Yersinia (inflammatory)
EHEC (non-inflammatory)
(Inflammatory = pos leukocytes in stool)
Dx of stridor and barking cough
AND/OR
Steeple sign on neck film
Parainfluenza (80% - mild)
RSV (15% - severe)
- hospitalized
Adenovirus
Influenza virus
Dx associated with dermatitis herpetiformis?
Antibody?
Celiac sprue
Tissue transglutaminase (anti-TTG)
Dx of Port Wine stain
Can be normal and resolve shortly after birth
OR
Sturge-Weber
- congenital anomaly of neural crest derivatives
=> capillary vascular malformations in CN V1/V2 distribution
- angiomas in retina and brain
Dx of Café au lait spots
Can be normal and resolve shortly after birth
Or rule out:
- neurofibromatosis type 1
(AD, Chr 17)
(Pigmented iris hamartomas, optic glioma, pheochromocytoma, seizures)
- McCune Albright Syndrome
(Gs protein activating mutation)
(Unilateral café au lait spots & at least one endocrinopathy)
Dx of collection of melanocytes in sacral area
Mongolian spots
- normal in people of color
- typically self resolve after a couple months
- or persists without complications
Dx of morbiliform rash
(= flat, red/pink spots that merge and become raised)
Rubeola
(2w measles)
- 3 C’s: cough, coryza, conjunctivitis
- Koplik spots
- SSPE (= subacute sclerosing panencephalitis)
Rubella
(3d measles)
- lymphadenopathy behind ears and neck
Dx that presents as RA but resolves 2 weeks later
Parvovirus B19
- fifth disease
- aplastic anemia
- red lacy rash appearance on cheeks (= slapped cheeks)
Rubella
(3d measles)
- lymphadenopathy behind ears and neck
- morbiliform rash
Dx associated with rash that presents as a red macule THEN clear vesicles THEN pustules and THEN scarring
Varicella
Chicken pox
Very itchy
Incr risk of skin infection
-> d/t scratching
1) staph aureus
2) strep pyogenes
Dx of painful ulcers in back of mouth, soles of feet, and palms
Coxsackie A
Hand-Foot-Mouth disease
MCC of bacterial meningitis
- 0-2 months
- 2mo - 10y
- 10-21 years
- >21 years
- immunocompromised
- strep agalactiae
- strep pneumo
- strep meningitis
- strep pneumo
- cryptococcus neoformans (presence of lymphocytes)
Common cold causes and how to differentiate
Rhinovirus -> nose only
Coronavirus -> spring/summer
Adenovirus -> fall/winter
- conjunctivitis
- swimming pool
Herpesvirus -> attacks cornea and gums
Influenza virus -> Nov-Feb; Cryoglobulinemia
Parainfluenza -> barking cough
Identify the meningitis:
1) pos proteins, neutrophils, decr glucose
2) pos proteins, T cells and macrophages, decr glucose
3) pos proteins, T cells and macrophages, norm or elev glucose
1) Bacterial
- strep pneumo
- strep agalactiae
- N meningitidis
2) TB/Fungal
- coccidiodomycosis
- cryptococcus neoformans
3) Viral (aseptic)
- enterovirus
- picorna
Viral causes of encephalitis
Arboviruses
- Birds -> Mosquito -> Human
- St Louis encephalitis
- Equine Eastern Encephalitis
*more E’s = more fatal
Herpesvirus
- prefers temporal lobe
