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118 Cards in this Set
- Front
- Back
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TPR =
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mean BP/CO
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Clearance is...
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ckearabce = urine flow * urine concentration/plasma concentration
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Test to determine diffusion coefficienct
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DLCO test, use inhaled CO with single respiration, measures diffusion cpacity
increased with recrutiement and dilation of pulmonary cpaillaries decreased with intersital lung disease, emphysema, and VQ imbalance |
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Patients with high lung compliance, which have low?
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COPD is high
restrictive lung disease has low |
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Differnece between relative and absolute refractory period
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absolute- Na channels inactivated and no AP can start
relative- some have recovered but requires a strnger stimulus |
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Calcium channels that are fun
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ryanodine receptor intracellular Ca release and also continuation of AP after start of funny channels in cardiac thing phsae 0
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secondary active transport
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can transport against gradient if coupled with something moving down a gradient like sodium gluclose or sodium aa transporters
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ras cascade
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activated by tyrosine kinase, activates ras -> raf -> MAPK cascade
insulin and growth factors work this way |
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Gi vs. Gs vs Gq receptors
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Gi inhibits adenylate cyclase, decrease cAMP
Gs stimulates adenylate cyclase to increase cAMP Gq activates phospholipase C goes to IP3 DAG protein kinase C pathway |
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Nerve fibers in order of diameter and velocity
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efferent to muscles, afferent from muscle spindles Aa, Ay efferent to muscel spindle
AB, Ad- afferent, touch, fast sharp pain C slow dull pain B and C effernt autonomics |
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Spinothalamic tract vs. dorsal columns
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dorsal columns- pressure form Merkels, light touch from meissners, vibraiton from pacinia
spinothalmic- pain and temp |
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Myopia vs. hymermetropia vs. presbyopia
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ppresbyopia- lens loses elasticity cannot shorten to focal length (become farsighted
Hymertropia- focal point too far (far sited) myopia- normal lleasciticty, focal point to short |
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nerar object
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ciliary muscle contracts, lens rounds, zonula fibers relax
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Pathologic nystagmus
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horizontal- vestibular disease
vertical- brainstem disease |
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Conductive vs. nerve deafness
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conducive- sound lateralizaiton to sick ear, boen conduction better than air, chronic otitis
nerve deafness air conduction bettern than bone, sound lateralizes to normal ear nerve disease |
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parasympatheyic and bladder
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causes emypting, relaxes internal sphincter, same with rectum
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Cholinercic receptors
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nicotinc- at ganlia, adrnela medulla, NMJ, ligand gate cation channel
muscarnic M1,3- PLC ->IP3 and DAG M2,4 ->inhbit adenylate cyclase -> camp decrease |
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adrenergic receptor tpes
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alpha 1- excitatory in vessels inhibitory in GI, Gq -> PLC -> IP3 DAG
alpha 2- CNS and presynaptic synmaptheitcs, Gi inhbits adeylate cyclase Beta 1 and beta 2 act via Gs Beta 1 excitatroy to heart beta 2 inhibtory on vessles and lungs |
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Epinephrine injection on heart
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increased conductio and contraction, increased frequency
increased systolic pressure with vasodilation causing decreased diastolic (norepi increases diastolic) |
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Muscle spindle vs. golig tendon organ
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muscle spindle measures lengt, actiavtes motorneuron when stretched
Golgi tendon organ0 measures tension, inhibits motorneuron |
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Decerebrate posture vs. decorticate psoture
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decorticate- brought to the core, arms legs flexed, cortex injury
decerebrate- brainstem, arms and legs extended |
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isometric contraction
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force increases but muscle length remains constant
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tonic vs. phasic smooth muscle
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tonic- vascular smooth muscle
phasic visceral smooth muscle, slow waves, spikes calcium calmodulin leads to MLC phsophorylation |
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n cardiac cycle a wave, c wave and v wave
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a wave- atrial contraction
c wave- bulging of mitral valve in sytole v wave filling of atria |
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How to determine dead space and residual volume
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dead space- anatomsicla dead space and unperfused alveoli, measured by nitrogen exhalation
RV measued by helium dilution or body pelthymography |
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COPD hypoxic drive
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central CO2 receptors not as responsive
peripheral O2 receptors become more important, can make the patient stop breathing |
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Cholinercic receptors
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nicotinc- at ganlia, adrnela medulla, NMJ, ligand gate cation channel
muscarnic M1,3- PLC ->IP3 and DAG M2,4 ->inhbit adenylate cyclase -> camp decrease |
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adrenergic receptor tpes
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alpha 1- excitatory in vessels inhibitory in GI, Gq -> PLC -> IP3 DAG
alpha 2- CNS and presynaptic synmaptheitcs, Gi inhbits adeylate cyclase Beta 1 and beta 2 act via Gs Beta 1 excitatroy to heart beta 2 inhibtory on vessles and lungs |
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Epinephrine injection on heart
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increased conductio and contraction, increased frequency
increased systolic pressure with vasodilation causing decreased diastolic (norepi increases diastolic) |
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Muscle spindle vs. golig tendon organ
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muscle spindle measures lengt, actiavtes motorneuron when stretched
Golgi tendon organ0 measures tension, inhibits motorneuron |
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Decerebrate posture vs. decorticate psoture
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decorticate- brought to the core, arms legs flexed, cortex injury
decerebrate- brainstem, arms and legs extended |
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isometric contraction
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force increases but muscle length remains constant
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tonic vs. phasic smooth muscle
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tonic- vascular smooth muscle
phasic visceral smooth muscle, slow waves, spikes calcium calmodulin leads to MLC phsophorylation |
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n cardiac cycle a wave, c wave and v wave
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a wave- atrial contraction
c wave- bulging of mitral valve in sytole v wave filling of atria |
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How to determine dead space and residual volume
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dead space- anatomsicla dead space and unperfused alveoli, measured by nitrogen exhalation
RV measued by helium dilution or body pelthymography |
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COPD hypoxic drive
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central CO2 receptors not as responsive
peripheral O2 receptors become more important, can make the patient stop breathing |
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Injury below the pons results in
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irregular fast deep respiration, below medulla all respiration stop
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Clopidorgrel MOA
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inhbits ADP-mediated platelet aggregation, used in those with stents or at risk for CVA or MI
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Eptifibatibe, abciximab, tirofiban
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glycoprotein IIbIIIa antagonsits, creates situation like Glanzmann's thrombocenia- stops platelet/platelet aggregation
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Fondaparinaux vs. heparin vs. LMWH
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fondaparinaux- only part of a heapain, binds to antithrombin selevtively inhibts factor X
heparin- binds to antithrombin to increase its inhibiton of IX, X< XI and XII needs to be monitored LMWH- doesn;t need to be monitored but an;t be reversedmainly acts of factor 10 |
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Streptokinase and urokinase
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streptokinase activates palsminogen- also catalyzes degradation of fibrinogen (I), V and VII
Urokinase activated plasminogen to degrade fibrin, less antigenic |
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tPA
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ateplase, only activates plasmin bound to fibrin, targets areas where clot formaiton has begun, targeted treatment
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Class 1 antiarryhmics serve as sodium channel blockers compare 1A, 1b, 1C
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1A- procainamide, quindine, can be used for ventricular or SVTs, slow phase 0 depolarization, prolong QT
1B- lidocaine, mildly slows phase 0, shorten phase 3, minimize abormal arryhmaias from abnormal automaticy not increased rate 1C- flecanide- decrease ectopy, very pro-arryhtmic, more prgound effect on phase 0 |
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Class II antiarryhtmics
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SURPRISE! BBs
slow heart rate by suppresing phase 4, diminsihs automaticity usefsul fro a fib, flutter, AVNRT |
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CCBs as antiarrryhtmics
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slow calciu conduction in AV node, slow phase 4 leading to a prolonged AP, decrease inward current carried by calcium, control ventricular rates in a fib
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Amiodarone
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K channel blocker, blocks outflow during repolarization, prologs AP and increases phase 3 depolarization, phase 0 unchanged, first line for many VT and SVTs, pulmonary fibrosis and thyroid probs
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MOA of digoxin
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blocks Na/K ATPase leads to rise in intracellular sodium, indirectly causing decreased exchange of Na for Ca, leads to increased Ca in cells, increased contractility
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First signs of tox of digoxin
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vision changes, nausea
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Dobutamne and dopamine
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B1 agonist action actiavtes adenyly cyclase to increase cAMP, this increases protein kinase leading to phsophorylation of calcium channels which leads to increased intracellualr caclium
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PDE inhibtors as inotropes
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milrinone, inamrinone
PDE inhibits convertion of cAMP to AMP, increased cAMP in cells prolongs action of protein kinase leading to increased intracellular calcium |
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Categories of asthma and their tx
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intermittent- FEV1 > 80, < 1 week, short acting beta 2
mild inermittent- more than once a week, inhlaed glucocortiocoids plus beta 2 agonist as needed moderate persistent- 60-80% FEV1, daily probs, nhaed roids, long acting beta 2s severe persistent- inhaled roids plus inhaled beta 2s long acting plus oral roids, possible omalizumbab |
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4 causes of asthma
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intrisinc- not allergy rleated, occur w/ stress or URI
extrinsic- most common d/t type I hypersensitivity exercise induced- inadequate symapthetic response drug- induced- self explanatory |
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Long acting and short acting beta 2 agonsits
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albuteol and terbulalaine, can decrease serum K
formoterol and salmetrerol are long lasting, associared with increased risk of death used chronically |
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cromolyn
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mast cell stabilizer for asthma rophylaxis. not for acute attacks
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Inhaled steroids
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beclomethasone, triacinolone, flunisolide, decrease prostaglandins and leukotrienes, inflammation
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Omalizumab
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monoclonal antibody to IgE, can cause anaphylaxis, used only for severe asthma
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leukotrienet inhibtiros
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prevent bornchoconstriciton, zileuton (blocks lipoxygenase), zafirlukast, montelukast (block the leukotriene receptor)
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methylxanthines
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theophylline, used as a PDE inhibitor to increase cAMP relieving airwflow obstruciton, low therapeutic index
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Buffalo hump, moon facies, truncal obestiy, HN, hyperglycemia. pituitary mass. Dx?
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Cushin's DISEASE
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Acromegaly vs. gigantism
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acromegaly occurs after adolescenec, don't grow tall, just grow bigger hands feet and head
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Etiology of PCOS
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overproduction of LH, not d/t pituitary adenoma, see hi LH and testosterone and estrone with low FSH
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SIADH
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overproduction of ADH, leads to hyponatremia and cerebral edema, possible HTN
small cell lung CA or head truauma |
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Causes of panhypoitutarism
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pituitary tumor
Sheehan;s syndrome TSH, GH, ACTH, LH, FSH all low |
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Patient presents with HTN and muscle weakness. Labs reveal hyponatremia. what is the problem and cause of the weakness?
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hypokalemia is the cause of the weakness
the disease in Conn syndrome |
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Child under 3 present with enlarging abdomen, cancer concern?
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neuroblastoma, from neural creast cells, may cause mets and ostructive problem, diarrhea d/t vasoactive intestinal peptide
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Patient presents with muscle weakness, hypotension and ... hyperpigmentation. Dx?
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Addison's disease
decreaseed aldosterone leads to hypotension and hyperkalemia, exces pituitary prduction of POMC leads to excess ACTH and melanocytte stimulating hromone |
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Ovarian tumor associated with hyperthyroidism?
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struma ovarii, ovarian teratoma, produces thyroid hromone, see hgih T3/T4, low TSH
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Patient has + anti-microsomal antibodies...
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Hashimotos, antithyroid, anti-thyroglobulin antibodies
leads to destruction of thyroid |
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Patient following viral URI, has malaise, feverer, thyroid enlargment and tender...
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DeQuervain's thyroidits, subacute thyroidiits
transient, tx w/ NSAIDs |
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Carcinomas of the thyroid
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mroe often in females, usually painless euthyroid mas, cold nodules
paillary, folliclr, anaplastic and medullary |
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4 types of thyroid carcinoma
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papillary- most common, good prognossis, psammona body, finger like projections
folliculr- middle aged, worse prognosis anaplastic- very agressive, old folks Medullary- elderly, tumor of parafolicular C cells, make calcitinon, leading to hypocalcemia d/t increased bone deposition, associated with MEN 2 |
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Roles of PTH
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activates osteoclasts, increasees renal reabsoprtion of CA, increases vitamin D, incfeases PO4 sexcretion, increases GI absorption
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Primary vs. secondary hyperparathyroidism
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primary- hi PTH, hi Ca lo PO4, d/t path of parathyroid
secondary- low calcum with response by paratyhroid, chronic renal failure, hi PTH, lo Ca, hi PO4 |
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pseudohypoparathyroidism
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PTH receptors non functional, tissues that PTH stimulates do not respond, hi PTH, low calcium and hi PO4, similar to hypoparathyroidism but PTH is high
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hypocalcemia in CRF
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decreased phsphate excretion, decreased active vit D production, increased PTh
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Hyperosmolar nonketotic coma
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enormous glucose lveles makes blood hyperosmolar causes water to enter blood and dessicate brain
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Ketoacidosis
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lack of insulin + stress leads to hormone overactivation of hromone sesnitive lipase leading to explosive lipolysis leading to ketoacids
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Gestational diabetes
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inadequate reserve for deans of pregnancy, juman placental lactogn from palcenta causes mild resistance to insulin
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Buffalo hump, moon facies, truncal obestiy, HN, hyperglycemia. pituitary mass. Dx?
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Cushin's DISEASE
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Acromegaly vs. gigantism
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acromegaly occurs after adolescenec, don't grow tall, just grow bigger hands feet and head
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Etiology of PCOS
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overproduction of LH, not d/t pituitary adenoma, see hi LH and testosterone and estrone with low FSH
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SIADH
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overproduction of ADH, leads to hyponatremia and cerebral edema, possible HTN
small cell lung CA or head truauma |
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Causes of panhypoitutarism
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pituitary tumor
Sheehan;s syndrome TSH, GH, ACTH, LH, FSH all low |
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Patient presents with HTN and muscle weakness. Labs reveal hyponatremia. what is the problem and cause of the weakness?
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hypokalemia is the cause of the weakness
the disease in Conn syndrome |
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Child under 3 present with enlarging abdomen, cancer concern?
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neuroblastoma, from neural creast cells, may cause mets and ostructive problem, diarrhea d/t vasoactive intestinal peptide
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Patient presents with muscle weakness, hypotension and ... hyperpigmentation. Dx?
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Addison's disease
decreaseed aldosterone leads to hypotension and hyperkalemia, exces pituitary prduction of POMC leads to excess ACTH and melanocytte stimulating hromone |
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Ovarian tumor associated with hyperthyroidism?
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struma ovarii, ovarian teratoma, produces thyroid hromone, see hgih T3/T4, low TSH
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Patient has + anti-microsomal antibodies...
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Hashimotos, antithyroid, anti-thyroglobulin antibodies
leads to destruction of thyroid |
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MEN Type I
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APPP- Werner's syndrome
Adrenal cortex- Conn, Cushing, virilization Pancreas (gastrinoma, insulinoma), parathyroid, pituitary) |
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MEN Type IIa
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Sipple's ATP
Adnreal medulla- pheochromocytoma Thyroid medulla- calcitonin Paraythyroid |
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MEN Type IIb
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ATMM
Adrnela medulla Thyroid medulla Marfanoid features, mucosal neuromas |
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Tests for thoracic outlet syndrome
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Adson's- patient extends elbow abducts arm and turns head ipsilateral in depp inhalation + w/ ecreased pulse
Roos test- boosh |
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Most common brachial plexus injury
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**Erb-Ducchene- C5-6
Klumnkes C8-T1- intrinsic muscle to hand injury |
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Adhesive capsiltis
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restriceted ROM of shoulder, gradully worse over time, immobility or guarding d/t trauma
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Posterior radial head
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stuck in pronation
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Muscle of the thumb not innervated by median nerve...
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adductor pollicis, flexor carpi ulnaris both innervated by ulnar nerve
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Thrombolytics
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activate plasminogen except tPA which activates plasmin leads to breakdown of fibrin
tPA selective for fibrin bound to plasmin |
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Cromolyn
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prophylaxis for asthma, prevents mast cell degranulation, not for acute attacks, only as an adjunct for tx of mild persistent asthma
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methylxanthines
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pDE inhibitors, increase cAMP, relieves airflow obstruction i chronic asthma
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ACE inhibitors in heart failure
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prevent cardiac remodeling d/t decreased Ang II levels, prevent progression
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BBs and heart failure
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prevent cardiac remodeling, decrease cardiac workload, decrease mortality
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what if there are changes in potassium in people on digoxin?
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low K can increase effects leading to tox
increased K can decrease effects |
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Digoxin affects HR, but how?
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increases vagal activity and sensitizes baroreeptors to decrease sympathetic response
no effect on mortality, just imporves sx and decreases hospital time can also be used to slow ventricular rate in A fib/flutter |
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Mech of vasodilators in CHF
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decrease preload, means decreased workload for heart and decreased edema
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postive inotropes for severe heart failure
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dobutamine- acts on B1 and B2- increased contractility w/o significant increase in rate
dopamine- increases renal pergusion, higher doses beta agonist, at high doses vasoconstriciton PDE inhibitors- inamrinone, milrinone- increases cAMP leads to vasodilation, velocity of relaxation, increase force of contraction |
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rate control vs. rhythym control
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rate- BBs, CCBs
rhythym- Na or K channel blockers |
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How can you stop AV nodal reentry?
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prolong refractory time, slow down rate in AV node
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How can you slow down Atrioventricular renetrent tachycardia in WPW? IS the QRS wide or narrow
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through AV node, narrow
blocking at AV node won't help need to block Na or K channels to slow accessory pathway |
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Sodium cahnnel blockers work in which parts of the heart?
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atria and ventriccles, not in AV node
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Lidocaine in ischemic tissue
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sodium channels open and drug binds, takes longer to come off, prolongs phase 0, less steep of a slope
less chance of arryhthmia then 1C (last longer affects normal tissue) |
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Quinidine, procainamdie, disopyramide
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Class 1A Na channel blockers
Quidine blocks Na cahannels prolong phase 0, block K prolonging repolarization, stops reentant circuits, a fib, ventricular arryhtmias has muscarinic affect that needs to be accoutned for in cardioversion |
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Lidoacaine MOA
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blocks fast Na channels, decreases phase 0 and action potential duration, and phase 4
mainly in ventricles |
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flecanide
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sodium channel block is more pronouced
can only be used without structural heart disease (previous MI or CHF), used for a fib and other stuff |
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Amiodarone
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blocks K channels prolongs AP duration, increases ERP
blocks inactivated Na cahannels, decrases conduction velocity, also blocks Ca channel, and alpha and B blocker too DOC for arryhtmias in patients with heart failure |
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What's the difference between amiodarone and dronedarone?
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donedarone does not have iodine so less toxic but... bad for severe heart failure
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will CCBs work in narrow QRS WPW?
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yes, decrease conduction velocity thorugh AV node and increased ERP in AV node, prevent reentry, but no good for a fib and WPW together
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adenosine MOA
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actiates adenosine receptors in AV ndoe, stops AV ndoal reentry
can be used for AVNRT and WPW |
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Mag sulfate as an antiarryhmic
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used for torsades, MOA unknown, suppresses EADs
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