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141 Cards in this Set
- Front
- Back
Mnemonic for hernias |
"MDs dont LIe"
MEdial to inferior epigastric artery= Direct hernia Lateral to inferior epigastric artery=Indirect hernia |
|
How many layers are involved in direct and indirect inguinal hernias?
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Indirect= all 3 layers of spermatic fascia (external spermatic, cremasteric, internal spermatic)
External= ONLY external spermatic fascia |
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What is the most common diaphragmatic hernia? describe it
|
Sliding hiatal hernia
GE junction is displaced "hourglass stomach) cardia normal (paraesophageal hernia is where cardia moves into thorax and GE jx normal) |
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what is the leading cause of bowel incarceration?
|
femoral hernia
more common in women protudes BELOW inguinal ligament through femoral canal |
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Indirect inguinal vs. Direct inguinal hernia
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INdirect:
goes thru INternal (deep) inguinal ring, external (superficial) inguinal ring, and INto scrotum INfants-due to failure of processus vaginalis to close Direct: bulges DIRECTLY thru abdominal wall MEDIAL to inferior epigastic artery (Hesselbach's triangle). Goes thru external (superficial) inguinal ring ONLY and covered by external spermatic fascia ONLY. older men. |
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What is contained in the femoral triangle vs the femoral sheath?
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femoral triangle: contains femoral nerve, artery, and vein
femoral sheath: contains the femoral artery, vein, and lymph nodes (deep inguinal) |
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What zone in the liver is affected 1st by viral hepatitis?
affected 1st by ischemia? has P-450 system? most sensitive to toxic injury? Alcoholic hepatitis? |
Zone 1: periportal zone
Zone 3: pericentral vein 1st by viral hepatitis? Zone 1 affected 1st by ischemia? Zone 3 has P-450 system? Zone 3 most sensitive to toxic injury? Zone 3 (i.e. acetaminophen) Alcoholic hepatitis? Zone 3 |
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Gastrin
what are potent stimulators? |
G cells (antrum of stomach)
increases gastric H+ secretion, increases growth of gastric mucosa, increases gastric motility phenylalanine and tryptophan are potent stimulators |
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CCK
what condition is assoc with CCK? |
I cells (duodenum, jejunum)
increases pancreatic secretion, increases gallbladder contraction, decreases gastric emptying pain worsening after fatty food ingestion in cholelithiasis due to increase in CCK |
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Secretin
|
S cells (duodenum)
increases pancreatic HCO3- secretion, increases bile secretion, decreases gastric acid secretion neutralizes gastric acid |
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somatostatin
what is it used to treat |
D cells (pancreatic islets, GI mucosa)
inhibits everything (gastric acid, pepsinogen, intestinal fluid, gallbladder, insulin, glucagon) used to treat VIPoma and carcinoid tumors |
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VIP
|
Parasympathetic ganglia in sphincters, gallbladder, small intestine
increases water/electrolyte secretion, increases relaxation VIPoma-non-a, non-B islet cell pancreatic tumor that secretes VIP, copious diarrhea |
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Gastrin
what are potent stimulators? |
G cells (antrum of stomach)
increases gastric H+ secretion, increases growth of gastric mucosa, increases gastric motility phenylalanine and tryptophan are potent stimulators |
|
CCK
what condition is assoc with CCK? |
I cells (duodenum, jejunum)
increases pancreatic secretion, increases gallbladder contraction, decreases gastric emptying pain worsening after fatty food ingestion in cholelithiasis due to increase in CCK |
|
Secretin
|
S cells (duodenum)
increases pancreatic HCO3- secretion, increases bile secretion, decreases gastric acid secretion neutralizes gastric acid |
|
somatostatin
what is it used to treat |
D cells (pancreatic islets, GI mucosa)
inhibits everything (gastric acid, pepsinogen, intestinal fluid, gallbladder, insulin, glucagon) used to treat VIPoma and carcinoid tumors |
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VIP
|
Parasympathetic ganglia in sphincters, gallbladder, small intestine
increases water/electrolyte secretion, increases relaxation VIPoma-non-a, non-B islet cell pancreatic tumor that secretes VIP, copious diarrhea |
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Nitric oxide
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increases smooth muscle relaxation
Loss of NO implicated in increased LES tone in achalasia |
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Motilin
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produced in small intestine during FASTING
causes MMCs (migrating motor complexes) |
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Ghrelin
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makes your stomach "Growl!"
increases GH, ACTH, cortisol, and prolactin secretion increases before meals and decreases after meals Regulates hunger lost following gastric bypass assoc w/hyperphagia in Prader-Willi |
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intrinsic factor
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parietal cells (stomach)- also produce gastric acid
Vit B12 binding, uptake in terminal ileum autoimmune destruction leads to chronic gastritis and pernicious anemia |
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gastric acid
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parietal cells (stomach)- also produce IF
stimulated by histamine, ACh, gastrin inhibited by somatostatin, GIP, prostaglandin, secretin Gastrinoma- results in high levels of acid secretion and ulcers |
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pepsin
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chief cells (stomach)
stimulated by vagal secretion and local acid converted from pepsinogen by H+ |
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HCO3-
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mucosal cells (stomach, duodenum, salivary glands, pancreas) and Brunner's gland (duodenum)
neutralizes acid it increases pancreatic and biliary secretion trapped in mucus that covers gastric epithelium |
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ECL cells
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produce Histamine which promotes the release of HCl from parietal cells (much more so than gastrin's direct effect on parietal cells)
stimulated by Gastrin |
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What stimulates salivary secretion?
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T1-T3 superior cervical ganglion (sympathetic)
facial (VII), glossopharyngeal (IX) nerve (parasympathetic) |
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What monosacharrides are absorbed by enterocytes?
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glucose, galactose, fructose
|
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What is taken up by SGLT1?
what mechanism |
glucose and galactose
via Na-dependent secondary active transport |
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What is taken up by GLUT-5?
what mechanism |
Fructose
facilitated diffusion since there is so much fructose in intestinal lumen |
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How are monosaccharides transported to the blood in enterocytes?
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via GLUT-2
|
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Where is iron, folate, B12, and bile acids absorbed?
|
Iron: duodenum
Folate: jejunum B12: ileum Bile acids: ileum |
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precursor of purines and pyrimidines?
|
purines: IMP precursor
pyrimidines: orotate precursor with PRPP added later |
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Antibiotic and anti-neoplastic drugs that function by interfering with nucleotide synthesis
Give mechanism |
Hydroxyurea: inhibits ribonucleotide reductase
6-MP: blocks de novo purine synthesis (purine antagonist) 5-FU: inhibits thymidylate synthase (decreases dTMP) MTX: inhibits dihydrofolate reductase (decreases dTMP) TMP: inhibits Bacterial dihydrofolate reductase (decreases dTMP) |
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Lesch-Nyhan syndrome
|
absence of HGPRT enzyme
excess uric acid production |
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Adenosine deaminase deficiency
|
excess ATP and dATP causing feedback inhibition
prevents DNA synthesis and decreases lymphocytes major cause of SCID |
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What happens with a mutation in nucleotide excision repair?
|
xeroderma pigmentosum
prevents repair of thymidine dimers caused by UV light |
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What happens with a mutation in mismatch repair?
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HNPCC (hereditary nonpolyposis colorectal cancer)
|
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What do lupus patients make antibodies to?
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Spliceosomal snRNPs
snRNPs combine w/pre-mRNA to remove introns by forming a spliceosome |
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total energy expenditure of adding one amino acid to peptide during translation
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4-phosphate bonds
t-RNA aminoacylation takes 2 phosphates from ATP->AMP |
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I-cell disease
|
inclusion cell disease
lysosomal storage disorder failure to add mannose-6-phosphate to lysosome proteins....causes enzymes to be trafficked out of cell FATAL in childhood |
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Drugs that act on microtubules
|
bendazole (antihelminthic)
griseofulvin (anitfungal) vincristine/vinblastine (anti-cancer) paclitaxel (anti-breast cancer) colchicine (anti-gout) |
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Chediak-Higashi syndrome
|
microtubule polymerization defect
results in decreased phagocytosis (since neutrophils divide quickly, less neutrophils) recurrent pyogenic infections partial albinism peripheral neuropathy |
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transport directions of dynein and kinesin
|
Dr. Ka
dynein: retrograde kinesin: anterograde |
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Kartagener's syndrome
|
dynein arm defect
results in immotile cilia causes infertility, bronchiectasis, recurrent sinusitis assoc w/ situs inversus |
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what is the cell type for these immunohistochemical stains
Vimentin Desmin Cytokeratin GFAP Neurofilaments |
Vimentin: connective tissue
Desmin: muscle Cytokeratin: epithelial cells GFAP: neuroglia Neurofilaments: Neurons |
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Ouabain
|
binds to K+ binding site of Na/K ATPase thus inhibiting Na+/K+ ATPase
|
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Digoxin and digitoxin
|
directly inhibit the Na+/K+ ATPase which leads to indirect inhibition of Na/Ca exchange
increases Ca2+ increases cardiac contractility |
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Ehlers-Danlos syndrome
|
faulty collagen synthesis
Type III collage affected assoc w/ hyperextensible skin tendency to blood (easy bruising) hypermobile joints |
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Osteogenesis imperfecta
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brittle bone disease
Autosomal dominant abnormal Type I collagen Multiple fractures w/ min trauma Blue sclerae |
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Alport's syndrome
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abnormal type IV collagen (imp in basement membranes)
X-linked recessive nephritis and deafness |
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Lyonization
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random x-inactivation in females
|
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Heteroplasmy
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presence of both normal and mutated mtDNA
results in variable expression of mitochondrial inherited disease |
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(P)rader-Willi syndrome
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deletion of normally active (P)aternal allele at imprinted locus of chromosome 15
mental retardation, hyperphagia, obesity, hypogonadism, hypotonia |
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angel(M)an's syndrome
|
deletion of a normally active (M)aternal allele at imprinted locus of chromosome 15
mental retardation, seizures, ataxia, inappropriate laughter "happy puppet" |
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Hypophosphatemic rickets
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X-linked DOMINANT-all female offspring of affected father are affected
increased phosphate wasting at proximal tubule results in rickets-like presentation |
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Leber's hereditary optic neuropathy
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Mitochondrial inheritance pattern: all offspring of affected females may show (due to heteroplasmy) signs of disease.
degeneration of retinal ganglion cells and axons leads to acute loss of central vision |
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Achondroplasia
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Autosomal Dominant
defect of FGFreceptor3 results in dwarfism head and trunk normal size |
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ADPKD
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Autosomal Dominant
defect in APKD1 on chromosome 16 (16 letters in polycystic kidney) always BILATERAL, present w/flank pain, hematuria, hypertension, progressive renal failure berry aneuryms, mitral valve prolapse |
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FAP
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familialy adenomatous polyposis
Autosomal Dominant colon covered w/ adenomatous polyps after puberty APC gene on chromosome 5 (5 letters in "polyp") progresses to colon cancer unless resected |
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Familial hypercholesterolemia
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Autosomal Dominant
defective or absent LDL receptor homozygotes worse than heterozygotes severe atherosclerotic dz early in life tendon xanthoma (achilles classically) |
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Hereditary hemorrhagic telangiectasia
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Autosomal Dominant
inherited disorder of blood vessels recurrent epistaxis, skin discolorations, AVMs (arteriovenous malformations) |
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Hereditary spherocytosis
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Autosomal Dominant
due to spectrin or ankyrin defect splenectomy is curative |
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Huntington's
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Autosomal Dominant, CAG trinucleotide repeat disorder ("Try Hunting MY FRIED X")
progressive dementia, choreiform movts, caudate atrophy, decreased levels of GABA and ACh symptoms manifest betw 20-50 chromosome 4 ("Hunting 4 food") |
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Marfan's syndrome
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Autosomal Dominant
Fibrillin gene mutation affects skeleton, heart, eyes dissecting aortic aneurysms, subluxation of lenses, floppy mitral valve |
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MEN
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Autosomal Dominant
Multiple endocrine neoplasias (1, 2A, 2B) familial tumors of Pancreas, Parathyroid, Pituitary, thyroid, adrenal 2A and 2B assoc with ret gene |
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Neurofibromatosis type 1 (von Recklinghausen dz)
Nf type 2 |
both Autosomal Dominant
Type 1: cafe-au-lait spots, neural tumors, Lisch nodules, scoliosis on chromosome 17 (17 letters in von Recklinghausen) Type 2: acoustic neuroma, juvenile cataracts NF2 gene on chromosome 22. Type 2=22 |
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Tuberous sclerosis
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Autosomal Dominant
adenoma sebaceum (facial lesions), ash leaf spots on skin, cortical and retinal hamartomas increased incidence of astrocytomas |
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von Hippel-Lindau dz
|
Autosomal Dominant
deletion of VHL gene (tumor suppressor) on chromosome 3 (3 words in VHL) results in constitutive expression of HIF and activation of angiogenic growth factors hemangioblastomas of retina/cerebellum/medulla, bilateral renal cell carcinoma |
|
X-linked recessive disorders
mnemonic? |
Be Wise, Fool's GOLD Heeds Silly Hope
Bruton's agammaglobulinemia Wiskott-aldrich syndrome Fabry's dz G6PD deficiency Ocular albinism Lesch-Nyhan syndrome Duchenne (and Becker's) muscular dystrophy Hunter's Syndrome Hemophilia A and B |
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Fragile X syndrome
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trinucleotide repeat disorder of CGG ("Try Hunting MY FRIED X")
defect of FMR1 gene Xtra-large testes, jaws, ears |
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Autosomal trisomies
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Down syndrome-trisomy 21 (Drinking age=21)
95% of cases due to meiotic nondisjunction of homologous chromosomes flat facies, epicanthal folds, simian crease increased risk of ALL and Alzheimer's Edward's syndrome-trisomy 18 (Election age=18) micrognathia (small jaw), clenched hands, death before 1 yr Patau's syndrome- trisomy 13 (Puberty=13) cleft lip/Palate, holoProsencephaly, Polydactyly, death before 1 yr |
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Cri-du-chat
|
microdeletion of short arm of chromosome 5
microcephaly, high-pitched crying (cry of the cat) |
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Williams syndrome
|
microdeletion of long arm of chromosome 7 (includes elastin gene)
distinctive elfin facies, mental retardation, hypercalcemia (increased sensitivity to vit D), extreme friendliness |
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22q11 deletion syndromes
|
CATCH-22
Cleft palate Abnormal facies Thymic aplasia Cardiac defects Hypocalcemia (parathyroid aplasia) 22q11 chromosome microdeletion due to aberrant development of 3rd and 4th branchial pouches DiGeorge syndrome: thymic, parathyroid, cardiac defects Velocardiofacial syndrome: palate, facial, and cardiac defects |
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What is bile needed for?
|
digestion of triglycerides and micelle formation in small intestine
|
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3 types of salivary gland tumors
|
generally benign and occur in parotid
pleomorphic adenoma: most common benign tumor, painless moveable mass Warthin's tumor: benign, salivary gland tissue trapped in lymph node Mucoepidermoid carcinoma: most common Malignant tumor |
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Where is the myenteric nerve plexus (Auerbach's) located?
Where is the submucosal nerve plexus (Meissner's) located? |
Myenteric nerve plexus (auerbach's): located in Muscularis externa
Submucosal nerve plexus (meissner's): located in Submucosa |
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what is responsible for lower esophageal sphincter relaxation?
|
VIP and NO
|
|
Achalasia
What can cause secondary achalasia? |
failure of relaxation of LES due to loss of Myenteric nerve plexus (lose smooth muscle motility)
dysphagia to both SOLIDS and LIQUIDS increased risk of ESOPHAGEAL CANCER bird's beak on barium swallow secondary achalasia is caused by Chagas' dz (destruction of ganglion cells by amastigotes) |
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GERD
|
heartburn and regurgitation upon lying down, also possible nocturnal cough and dyspnea
Complications: strictures, Barrett's esophagus |
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Esophageal varices
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PAINLESS bleeding of submucosal veins in lower 1/3 of esophagus (smooth muscle only)
caused by portal hypertension due to anastomosis betw LGV and EV |
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Mallory-Weiss syndrome
|
Mallory weiss tear!
PAINFUL mucosla lacerations at the GE jx due to severe vomiting usu found in alcoholics and bulimics |
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BoerHaave syndrome
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"Been Heaving syndrome"
TRANSMURAL esophageal rupture due to violent retching |
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Esophagitis
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assoc w/reflux, infection (HSV-1, CMV, Candida), or chemical ingestion
|
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Plummer Vinson syndrome
|
plummers "DIG" open clogs
Triad of: Dysphagia (due to esophageal webs-mucosa and submucosa protude into the esophageal lumen) Iron deficiency anemia Glossitis (inflammation/infection of the tongue) |
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BARRett's esophagus
|
BARR=
Becomes Adenocarcinoma Results from Reflux glandular metaplasia-replacement of non-keratinized stratified squamous epithelium with intestinal columnar epithelium in distal esophagus pre-malignant condition |
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What are the risk factors for esophageal cancer?
Locations for squamous cell ca and adenocarcinoma? |
"ABCDEF"
Achalasia/Alcohol Barrett's esophagus (greatest risk for adenocarcinoma) Cigarettes Diverticuli (e.g. Zenker's diverticulum) Esophageal web (PlumVsynd)/Esophagitis Familial presents as progressive dysphagia (solids then liquids) leading to wt loss Squamous: upper and middle 1/3 Adenocarcinoma: lower 1/3 |
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What is the most common benign tumor of the esophagus?
|
Leiomyoma
|
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Celiac sprue
Tropical sprue Whipple's disease |
All are malabsorption syndromes that can cause diarrhea, steatorrhea, wt loss, and weakness
Celiac sprue: autoantibodies to gluten, involves PROXIMAL small bowel primarily Tropical sprue: infectious (responds to antibiotics), can affect ENTIRE small bowel Whipple's disease: infection w/ Tropheryma whippelii (gram positive), PAS-positive macrophages in lamina propria, OLDER MEN |
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Pancreatic insufficiency
|
malabsorption of fat and fat-soluble vitamins (A, D, E, K)
due to cystic fibrosis, obstructing cancer, and chronic pancreatitis |
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Abeta-lipoproteinemia
|
decreased synthesis of apoB->
inability to generate chylomicrons-> decreased secretion of cholesterol, VLDL into bloodstream-> fat accumulation in enterocytes malabsorption and neurologic manifestations in early childhood |
|
Celiac sprue
|
autoimmune-mediated intolerance of gliadin (gluten) leading to steatorrhea and blunting of villi
antibodies to gliadin and tissue transglutaminase assoc w/dermatitis herpetiformis increases risk of malignancy |
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what is the most common tumor of the adrenal medulla in adults?
describe the effects |
pheochromocytoma, derived from chromaffin cells
secretes excessive amts of the catecholamines (epi, NE, dopamine-all tyrosine-derived) causes episodic HTN VMA (breakdown product of NE) in urine |
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most common adrenal tumor in children
|
neuroblastoma
can occur anywhere along the sympathetic chain HVA (breakdown product of dopamine) in urine N-myc oncogene |
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What is secreted by adrenal medulla? by what cells specifically? what is the primary regulatory control?
|
catecholamines
by chromaffin cells controlled by preganglionic sympathetic fibers |
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What is secreted by zona glomerulosa, fasciculata, reticularis?
what is the primary regulatory control for each? |
GFR: Salt, sugar, sex
Glomerulosa: aldosterone controlled by renin-angiotensin system Fasciculata: cortisol, sex hormones controlled by ACTH, hypothalamic CRH Reticularis: sex hormones (androgens) controlled by ACTH, hypothalamic CRH |
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Adrenal gland drainage
Gonadal vein drainage |
Right goes directly into IVC
left adrenal vein-> left renal vein-> IVC left gonadal vein-> left renal vein-> IVC right adrenal vein-> IVC right gonadal vein-> IVC |
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NE can be converted into epinephrine by what enzyme
|
PNMT, which is stimulated by cortisol, mainly during periods of stress
|
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what is the rate-limiting step in Catecholamine synthesis ?
|
conversion of tyrosine to dopa by tyrosine hydroxylase
|
|
rate-limiting enzyme of glycolysis
|
What's #1 in glycolysis?
phosphofructokinase-1 (PFK-1) |
|
child presents with pellagra but is NOT niacin deficient
|
pellagra= diarrhea, dermatitis, dementia
Hartnup disease; due to a transport protein defect with increased excretion of neutral amino acids (tyrosine which is the precursor for the biosynthesis of niacin) |
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heavy smoker, severe pain, faint pulses. Raynauds, and gangrene of the toes/fingers
|
Buerger's Dz
small and medium vessel vasculitis |
|
child comes in with progressive neurodegeneration, hepatosplenomegaly, and cherry-red spot on macula.
what dz? what is the deficiency? What if pt had no hepatosplenomegaly? |
Niemann-Pick dz, a lysosomal storage dz
sphingomyelinase is deficient, so sphingomyelin accumulates What if pt had no hepatosplenomegaly? Tay-Sachs (hexosaminidase A deficiency) |
|
pt has sever fasting hypoglycemia, highly elevated glycogen in liver, increase in blood lactate and hepatomegaly.
what does pt have? what is the deficiency? What if if was milder presentation with NORMAL blood lactate levels? |
Von Gierke's disease (type I), glycogen storage dz
Glucose-6-phosphatase is deficient milder presentation with NORMAL blood lactate levels? Cori's dz (type III)-defective debranching enzyme (a 1-6 glucosidase); gluconeogenesis is intact |
|
child presents with progressive neurodegeneration, developmental delay, cherry-red spot on macula, lysosomes with onion skin, but no hepatosplenomegaly?
What is dz? what is the deficiency? |
Tay-sachs, a lysosomal storage dz
hexosaminidase A deficiency, leading to accumulation of GM2 ganglioside |
|
Pompe's dz
|
deficiency of lysosomal a-1-4 glucosidase (acid maltase) Type II glycogen storage dz
cardiomegaly and systemic findings leading to early death "Pompe's trashes the Pump" (heart, liver, muscle) |
|
McArdle's dz
|
Mcardle's=MUSCLE
deficiency of skeletal muscle glycogen phosphorylase, Type V glycogen storage dz increased glycogen in muscle, but can't be broken down painful muscle cramps and myoglobinuria w/strenuous exercise |
|
What endocrine hormones use the cAMP signalling pathway?
|
"FLAT CHAMP GCG"
FSH LH ACTH TSH CRH hCG ADH (v2 receptor) MSH PTH GHRH Calcitonin Glucagon |
|
What endocrine hormones use the IP3 signalling pathway?
|
"GOAT"- all made in hypothalamus
GnRH Oxytocin ADH (v1 receptor) TRH |
|
Cushing's syndrome
exogenous and endogenous causes |
increased cortisol
Exogenous: steroid; #1 cause, low ACTH Endogenous 1.Cushing's dz; secretion from pituitary adenoma, high ACTH 2.Ectopic ACTH; nonpituitary tissue making ACTH, high ACTH 3. Adrenal; adenoma, carcinoma, adrenal hyperplasia, low ACTH Dex suppression test to determine cause: both Ectopic and Adrenal will have high cortisol after both low and high doses of dex |
|
What is Conn's syndrome?
what are the findings? What is the treatment? |
primary hyperaldosteronism caused by aldosterone-secreting tumor
hypertension, hypokalemia, metabolic alkalosis, LOW renin Tx: Spironolactone |
|
What is secondary hyperaldosteronism?
|
kidney perception of low intravascular volume resulting in overactive RAAS; HIGH plasma renin
due to renal artery stenosis, CHF, nephrotic syndrome, chronic renal failure, cirrhosis |
|
Addison's Disease
|
CHRONIC adrenal insufficiency
Primary: due to adrenal atrophy/destruction where no cortisol or aldosterone is produced, excess ACTH is produced causing hypotension and skin hyperpigmentation (MSH) Secondary: due to prob with pituitary where little ACTH is produced; no hyperkalemia and no hyperpigmentation Waterhouse-Friderichsen syndrome is ACUTE adrenocortical insufficiency |
|
Waterhouse-Friderichsen syndrome
|
ACUTE adrenocortical insufficiency due to adrenal hemorrhage
assoc w/ N. meningitidis septicemia, DIC, and endotoxic shock |
|
what are the 5Ps in pheochromocytoma
|
since it is a tumor of adrenal medulla which secretes catecholamines (epi, NE, dopamine)
elevated blood Pressure Pain (headache) Palpitations (tachycardia) Perspiration Pallor |
|
Jod-Basedow phenomenon
|
Jod=iodine in German
hyperthyroidism (thyrotoxicosis) that can occur after iodine/iodide administration in a person w/iodine deficiency goiter |
|
Causes of hypercalcemia
|
"CHIMPANZEES"
Calcium ingestion (milk-alkali syndrome) Hyperparathyroid Hyperthyroid Iatrogenic(thiazides) Multiple myeloma Paget's disease Addison's disease Neoplasms Zollinger-Ellison syndrom Excess vitamin D Excess vitamin A Sarcoidosis |
|
how do you treat prolactinoma?
what can it impinge on and cause? |
give bromocriptine or cabergoline (dopamine agonsists) since dopamine from the hypothalamus normally inhibits prolactin production allowing GnRH to stimulate spermatogenesis and oogenesis
cause shrinkage of pituitary adenoma can impinge on OPTIC CHIASM causing BITEMPORAL HEMIANOPIA |
|
what can be given to prevent mast cell degranulation in asthma?
|
Cromolyn sodium
|
|
when do you see hypersegmented polys (PMNs/neutrophils)?
|
folate/B12 deficiency
macrocytic anemia |
|
what drug inhibits COX and why is that important?
|
aspirin
inhibits formation of TsA2. |
|
what drug inhibits ADP-induced expression of GpIIb/IIIa
|
clopidogrel and ticlopidine
|
|
what drug inhibits GpIIb/IIIa directly
|
Abciximab
|
|
What has the classic triad of iron deficiency anemia, esophageal webs, atrophic glossitis (smooth, painful tongue)
|
Plummer vinson syndreom
|
|
What bugs do NOT gram stain well
|
"These Rascals May Microscopically Lack Color"
Treponema (too thin) Rickettsia (intracellular parasite) Mycobacterium (high lipid content wall requires acid-fast stain) Mycoplasma (no cell wall) Legionella (intracellular) Chlamydia (intracellular parasite) |
|
What does Giemsa stain
|
Giemsa is for parasites like BPC and trypanosomes
BPC-Borrelia, plasmodium, chlamydia |
|
What does PAS stain detect
|
Whipple's Dz
different types of glycogen storage disease Paget's disease diagnose α1-antitrypsin deficiency if periportal liver hepatocytes stain positive. |
|
what can india ink be used for
|
cryptococcus
|
|
what can silver stain be used for
|
Legionella
Fungi |
|
What are the only gram positive organisms?
|
Staph, strep -> cocci
bacillus, clostridium, Corynebacterium, listeria, mycobacterium (think TB+, gram +) -> bacilli Actinomyces israelii, nocardia ->branching filamentous |
|
Culture for H flu
|
Chocolate agar w/ factors V and X
I eat chocolate 5-10 times a day when I have H. flu! |
|
Culture for N. gonorrhoeae
|
Thayer-Martin or
VPN media to connect to Neisseria, use your VPN client |
|
Culture for Bordetella pertussis
|
Bordet for Bordetella
Bordet-Gengou agar |
|
Culture for C. diptheriae
|
Tellurite or Lofflers media
T-Lo for Dipth |
|
Culture for M. tuberculosis
|
Lowenstein-Jensen agar
J-Lo has Tb! |
|
Culture for M pneumoniae
|
Eaton's agar
EatON my pneumonia! |
|
Culture for Lactose-fermenting enterics
|
MacConkey's agar (pink colonies)
Klebsiella, E. coli Enterobacter, citrobacter, serratia |
|
Culture for Legionella
|
charcoal yeast extract agar
|
|
Fungi
|
Fungi are Sabor!
Sabouraud's agar |
|
What are the obligate aerobes?
|
"Nocardia Pathogens Must Breath"
Nocardia Pseudomonas Mycobacterium tuberculosis Bacillus |
|
What are the obligate anaerobes?
|
anaerobes Can't Breath Air
Clostridium Bacteroides Actinomyces normal flora in GI tract aminO2glycosides are ineffective bc need O2 in order to enter bacterial cell |