Physiology Flashcards
mechanism for PTH
1) work via its R on osteoblasts by indirect mechanism ⟹ increase RANK ligand, M-CSF ⟹ osteoclast presursor diff into mature ⟹ bone reabsorption
2) inhibits the release of osteoprotegrin (a decoy for RANK ligand receptor, which impeded the RANK interaction)
net result for PTH: Ca2+ re-absorption, urine excretion of P
function of calcitonin
made by thyroid gland; inhibits osteoclast, decrease bone reabsorption, increase bone mineral density;
effect opposite to PTH
ECG presentation for AF?
No P-wave (no regular atrial contraction); replaced by “f-wave” (fibrillatory)
narrow QRS wave, inregular R-R interval
In AF, the determinant for ventricular contraction rate is the AV node refractory period
Kartagener’s syn
microtubular dynein arm defect: immotile cilia
infertility, recurrent sinusitis, bronchiectasis
卡特在戛纳：不孕症
cardiac abnormality associated with Downs?
ASD
failure of the endocardial cushions of the AV canal to fuse completely ; patients usually also have cleft in the anterior MV and in the septal leaflet of the TV ⟹ AV regurgitation
DiGeorge Syn
乔治弟弟没胸没屁屁（无胸腺）, 没法乐死 （associated with TOF)
chr 22q11.2 deletion: thymic aplasia, failure of parathyroid formation from the defective 3rd and 4th pharyngeal pouches
hypocalcemic tetany, recurrent viral and fungal infections (no T cells); TOF!!!
Wegener’s disease
vs. Churg-Struass Syn
瓦格纳一看美女就流鼻血，其实是个肾衰的中性人
C-ANCAs, cytoplasmic-staining anti-neutrophil cytoplasmic Ab) cause granulomatosis with polyangiitis
Px: nectrotizing vasculitis of the upper and lower RI (nasal ulceration, sinusitis, hemoptysis) + rapidly progressive glomerulonephritis (produce RF)
斯特劳斯和瓦格纳对应（p-ANCA),
斯特劳斯有多动症（写了太多圆舞曲），神经质而且过敏
成人哮喘及过敏，嗜酸性粒细胞增多，多动脉炎，单、多神经炎，付鼻窦
Dx: wide, split S2?
characteristic for ASD
most important damage: pulmonary HT (can cause reversed R-L shunt: late onset cyanosis - Eisenmenger Syn)
Lambert-Eaton syn
autoimmune paraneoplastic syndrome, myasthenic symptoms, Ab against presynaptic Ca2+ channel can’t release Ach
often associated with small cell lung cancer
AFR (acute rheumatic fever)
Px: heart? CNS?
Dx criteria?
heart: days to 6 wks after “sore throat”: vegetation on MV, AV
CNS: Sydenham chorea, 2-3 mo after streptococcus infection
Dx requires 2 major Jones criteria + 2 minor Jones criteria:
- Major: carditis, polyarthritis, chorea, erythema marginatum, s.c. nodules
- minor: fever, arthralgia, ↑ ERS or C-reactive protein, prolonged PR interval
H produced by the posterior pituitary gland?
- vasopressin: increase permeability of the renal collecting ducts to water ⟹ ↑ water reabsorption
- oxytocin
mechanism for Adenosine, Ach to reduce HR?
pacemaker AP:
- phase 0 (upstroke): opening of L-type (long-lasting) Ca2+ channel
- phase 3 (repolarization): opening of K+ channel
- phase 4 (pacemaker potential): 慢Na+通道开放, K+ channel close: - 50 mV, then T (transient)-type Ca2+ channel open: - 40 mV, L-type Ca2+ channel open
Adenosine and Ach activates K+ channels and inhibit L-type Ca2+ channels
心脏听诊：
- apex murmur
- mid systolic click?
- S2-to-opening snap time interval: indicator of?
- audible S3: indicate? - murmur at right sternal border
- holosystolic murmur at left sternal border; attenuate with the handgrip
- fixed splitting of S2
- continuous precordial murmur, during both diastolic and systolic:
- systolic, crescendo-decrescendo murmur, start after S1 and end before the A2 component of S2
- MV
MR: holosystolic murmur at apex, radiate to axilla (腋窝）- presence of audible S3 is the indicator of severity
mid systolic click? MV prolapse
S2-to-opening snap time interval: indicator of MV stenosis severity
-audible S3: in young patient: indicate severity of MV regurgitaiton; in older patients: ↑ LVESV (occurs in the setting of LV systolic failure)
- AV
if “crescendo-decrescendo” systolic murmur: aortic regurgitation - holosystolic murmur at left sternal border: VSD
(handgrip ↑ Afterload) - fixed splitting of S2: ASD
5: PDA (patent ductus arteriosus) - AS (aortic stenosis)
职业性肺病的histologic表现：
1。 nodular interstitial densities, mostly in the apical region; calcified hilar ndes, (eggshell calcification) + bifrefringent particles
- lower lobes, involvement of pleural + pleural effusion ; ferruginous bodies (beaded rods with iron-containing coat)
1。 silicosis
- asbestosis
Dx:
African American, malaise, nocturnal fevers, cough + bilateral hilar adenopathy + biopsy shows non-caseating granulomas
sarcoidosis
if caseating granulomas: TB
PaO2 threshold to develop hypoxic 2nd erythrocytosis?
65 mmHg (SaO2 < 92%)
mechanisms to clear the particles from airway:
- 10- 15 uM in size
- 2.5-10 uM
- < 2 uM
- cough and upper airway trapping
- mucociliary transport
- phagocytosis
major player in asthma?
IL-5 released by Th2 cells
activate eosinophils (granule-coated); “crystalloid bodies” - “charcot-Leyden crystals” (contain eosinophil membrane protein)
Among numerous inflammatory cytokines in asthma, pharamcological antagonists against only 2 of these cytokines are affective to control asthma: what are these 2 factors?
leukotrienes (LTC4, LTD4, LTE5)
Ach
What are the major mechanisms for hypoxemia? And what’s the A-a gradient in each case?
从肺泡 - 肺血流 - 体循环：
1、alveolar hypoventilation
- gas diffusion impaired
- V/Q mismatch
- R-L shunt
A-a is normal in 1, and ↑ in 2-4
Nephrotic vs. Nephritic syn: Which is associated with classic proteinuria (> 3.5 g/day)?
Nephrotic (o = pr”o”tein)
no inflammotory response; slight ↓ GFR
(ex: DM nephropathy)
- nephritic syn: RBC, WBC casts, active inflammatory response, significant ↓ GFR
(ex: Alport Syn, damage collagen in the basement mem)
In kidney, what substances are:
- only filtered, no reabsorption or secretion?
- filtered + re-absorption?
- filtered + reabsorption + secretion
- inulin, mannitol
- glucose, Na+, urea
- PAH (para-aminohippurate, 对氨基马尿酸盐）， creatinine
肾功能常用计算：
GFR?
FF?
GFR = creatinine clearance
FF = GFR/ RPF (renal plasma flow)
RPF = PAH clearance
clearance of any substance = (urine concentration * urine flow rate)/ plasma concentration
If RBF is unknown, it can be calculated from RBF (renal blood flow):
RPF = RBF * (1-hematocrit)
which cell types have glucose transport that responds to insulin?
only skeletal muscle cells and adipocytes
among the 5 GLUTs, only GLUT4 is regulated by insulin. They locate in the cytoplasm of skeletal muscle cells and adipocytes, and translocate onto cell membrane with insulin
secretin:
cells produce this hormone? stimulator? function?
produced by S-cells in the duodenum (最容易被酸腐蚀）; respond to increased 【H+] in the duodenum.function: promote HCO3- secretion from pancreatic ductal epithelium to neutralize H+
pancreatic juicy: isotonic, [Na+], [Cl-] = plasma
[HCO3-] > plasma, [Cl-] < plasma
trypsinogen: converted by which E? where?
converted by enterokinase in the intestinal brush border; then active trypsin can also activate trypsinogen
secretion of pancreatic E (including trypsinogen) is stimulated by cholecystokinin and cholinergic stimulation
1 g protein = ? cal
1 g CHO = ? cal
1 g fat = ? cal
1 g protein or CHO = 4 cal
1 g fat = 9 cal
Zollinger-Ellison Syn
gastrinoma
tumor mostly locates in the distal duodonum, also in pancrease and the fudus of stomach; excess gastrin - HCL - ulcer
stimulators/inhibitors for gastric acid production?
stimulators: Ach, histamine, gastrin (associated with Zollinger-Ellison syn)
inhibitor: PGE2
producing cells of VIP? function of VIP?
produced in the pancrease
functions: stimulate intestinal water secretion, counteracts gastrin in the stomach; promote HCO3- secretion in the pancrease
somatostatin: producing cells? function?
= Growth hormone-inhibiting hormone 生长激素抑制素
produced by numerous tissues (hypothalamus, stomach, intestine, pancrease) in response to low pH
its production is inhibited by vagal stimulation
somatostatin inhibits the release of GH, TSH, gastrin, CCK, VIP, secretin, insulin, glucagon
