- diabetes causes - What causes type 1 diabetes?
destruction of the beta cells of the pancreas.
- diabetes causes - What causes type 2 diabetes
the body is unable to use insulin effectively. the beta cells of the pancreas produce insulin normally when the disease begins, but will eventually tire and not produce as much insulin.
- Diabetes and regional - ...kind of a vague study suggestion...
diabetics are more prone to infection. poorly controlled diabetics experience increased levels of post-op pain. diabetics are also typically dehydrated, so if you're doing a spinal, they may bottom out faster. (that's all i could find in the articles regarding regional and diabetes)
- diabetics and the reason they can become stiff - What is the reason diabetics become stiff?
i don't remember seeing this in the articles, but the reason is because the excess glucose floating around glycosylates with all of the cells of the body. this glycosylation or "activated glycosylated end-product" (AGE) thickens the cells and makes them stiff. that's why we check the HbA1C, because the RBCs have become glycosylated over the 3 month period prior. organs typically effected: kidneys, blood vessels, peripheral nerves, and lenses of the eye. (the way i learned it is that glycosylation is a non-enzymatic reaction that simply just occurs if there is too much glucose floating around for too long of a time. craziness.) wikipedia says it's an enzymatic reaction. whatever...
- carcinoid syndrome and the heart - Cardiac involvement has been reported in more than half of the patients with carcinoid syndrome. Cardiac lesions, if present, may result from the secretion of bioactive mediators and most often affect only the ______ side of the heart. What are the mediators and why only one side?
Right side of the heart is affected by fibrous thickenng of the endocardium and fixation of the tricuspid valve. The lungs have the ability to clear out the causative agents mediators: 5-HTP (serotonin) and substance P.
- carcinoid syndrome and the heart - Serotonin may cause vasoconstriction and vasodilation. Why?
At normal concentrations, serotonin does not affect cardiac function; however, the elevated levels seen in carcinoid syndrome may cause both inotropic and chronotropic responses. This action is due in part to an indirect effect from the release of norepinephrine.
- carcinoid tumors and medications to use and avoid - Medication used to treat the symptoms of any residual tumor remaining after surgery?
octreotide (this is a somatostatin. somatostatins block hormones)
- carcinoid tumors and medications to use and avoid - Release of _________ and _________ should be avoided when choosing which medications to use.
catecholamines and histamine (propofol and etomidate are good for induction; succs is debatable; don't use opioids that cause histamine release; only use NDNB that don't cause histamine release, vec is the best choice because of cardiac stability)
- carcinoid tumors and medications to use and avoid - Because these patients often have chronic right ventricular valvular lesions and heart failure, one should avoid anesthetic factors that increase RV work with potential precipitation of acute RV failure. What 3 factors does this include?
hypoxemia hypercarbia a light anesthetic plane
- carcinoid tumors and medications to use and avoid - What is the drug of choice for treating hypotension perioperatively in carcinoid tumor patients?
octreotide (IV boluses up to 1.0mg), along with fluids (hypotension can be a serious problem since the drugs usually used to treat hypotension may make it worse by further stimulating the release of peptides)
** For burn injury info, look at the other brainscape cards for burns **
.... no reason to rehash it since it was vague on the study guide ...
- anesthetics for the patient with muscular dystrophy - Duchenne muscular dystrophy and administration of Suc's, NDNMB and inhaled agents can trigger ?
Rhabdo and MH
- anesthetics for the patient with muscular dystrophy - Why can rhabdo or MH happen with muscular dystrophy patients? What is happening in the cell?
the absence of the dystrophin-glycoprotein complex results in instability and increased permeability of the sarcolemma and increased intracellular calcium levels. exposure of the sarcolemma to the potent inhalational agent (or succ's) stresses the muscle membrane and further increases the instability and permeability. consequently, intracellular calcium levels increase further and cell contents, such as potassium and CK, leak out. **a compensatory hypermetabolic response occurs in an attempt to reestablish membrane stability and prevent calcium fluxes. (this mechanism may explain the hyperkalemia, hyperthermia, tachycardia, and rhabdo observed in these patients. knowledge!)
- anesthetics for the patient with muscular dystrophy - Should you use inhalational agents or do a TIVA for these patients?
TIVA (a "trigger-free" anesthetic and a "clean" machine with the inhalational agents flushed out)
- anesthetics for the patient with muscular dystrophy - If anesthesia induced rhabdo is suspected, serial potassium levels should be measured and immediately treated if greater than ______ mmol/L. What is the treatment?
5.5 mmol/L treatment: IV sodium bicarb, insulin with 10% dextrose, and the patient hyperventilated to produce a respiratory alkalosis.
- anesthetics for the patient with muscular dystrophy - If anesthesia induced rhabdo is definitely happening, what additional steps need to be taken to protect the kidneys?
IV hydration and mannitol, to maintain the UOP > 1ml/kg/h
- anesthetics for the patient with muscular dystrophy - What is the treatment for perioperative hyperkalemic cardiac arrest?
IV calcium chloride (to antagonize the myocardial effects of hyperkalemia and help restore a spontaneous rhythm)
- Duchennes muscles issues, cardiac changes - Patients with Duchennes suffer from progressive degeneration of what types of muscle?
skeletal, cardiac, and smooth muscle (Lack of the dystrophin protein in muscle cells causes them to be fragile and easily damaged)
- Duchennes muscles issues, cardiac changes - _______ __________ occurs in over 50% of patients by 15 years of age.
- SLE confirmation and pulmonary issues/cardiac issues - What is the best diagnostic test for systemic lupus erythematous?
the antinuclear antibody (ANA) test (the ANA is positive in significant titer - usually 1:160 or higher)
- SLE confirmation and pulmonary issues/cardiac issues - SLE usually begins with one or several of the following features. (11)
-unexplained fever, fatigue, and weight loss -photosensitive rash (butterfly rash on face) -arthritis -raynaud phenomenon -serositis (pleuritis, pericarditis, peritonitis) -nephritis or nephrotic syndrome -neurologic symptoms, such as seizures, psychosis or stroke -alopecia -phlebitis -recurrent miscarriage -anemia
- SLE confirmation and pulmonary issues/cardiac issues - Which cardiac problem is relatively common with SLE?
pericarditis (side-note: verrucous [Libman-Sacks] endocarditis is usually clinically silent but can produce valvular insufficiency and serve as a source of emboli)
- SLE confirmation and pulmonary issues/cardiac issues - Do patients with SLE have an increased or decreased risk of coronary artery disease?
- SLE confirmation and pulmonary issues/cardiac issues - What are often considered the first clues either to lung involvement or to SLE itself? (3)
pleurisy, coughing, and/or dyspnea
- SLE confirmation and pulmonary issues/cardiac issues - What are some lung issues that can occur in SLE? (6)
pleurisy pleural effusion pneumonitis interstitial lung disease pulmonary HTN alveolar hemorrhage
- SLE confirmation and pulmonary issues/cardiac issues - What issues would suggest shrinking lung syndrome? (4)
dyspnea episodic pleuritic chest pain progressive decrease in lung volume in the absence of interstitial fibrosis significant pleural disease
- SLE confirmation and pulmonary issues/cardiac issues - Pulmonary function tests are often significantly abnormal prior to complaints of dyspnea. Do they show obstructive or restrictive abnormalities?
Geriatric, pulmonary: By age 70, your alveolar surface available for gas exchange has decreased by how much?
Geriatric, pulmonary: Why does your alveolar surface available for gas exchange decrease by 15% by age 70? (2 reasons)
1. Reduction of elastic tissue 2. Increased collagen
Geriatric, pulmonary: What happens to PaO2 when the alveolocapillary membrane thickness increases in elderly patients?