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OPT 537 - OWN > Renal System > Flashcards

Renal System Flashcards

1
Q

Chronic Kidney Disease

A

Structural or functional abnormality of the kidney for at least 3 months. >10% of US has chronic kidney disease

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2
Q

End Stage Renal Disease

A

Require a kidney intervention to stay alive. Those of african discent are 8X more likely

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3
Q

Ocular systems from renal disease

A

Calcium deposits on lid or conj, lid edema, corneal changes, aniridia (missing iris), cataracts, uveitis, ONH edema, drusen around the macula, retina changes

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4
Q

Optometric Considerations with renal disease

A

Optometric prescribed meds can cause renal side effects and dosage must be altered with renal disease. Renal disease also increase risk of ARMD, dry eye, and red eye.

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5
Q

Kidney Functions

A

Excretory: remove waste, regulate composition of blood (amt of water, [] of ions, acid-base balance) and excrete foreign substances.
Endocrine: involved with calcium output and regulation, erthropotient (development of RBC) and things like prostoglandins and nitric acid.

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6
Q

Renal Veins

A

Blood returns to heart through inferior vena cava

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7
Q

Renal artery

A

major branch from aorta. 20% received is filtered. Blood flows at about 1.2 l/min.

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8
Q

Ureter

A

Creates urine. Enters at hilus. Connectes kidney to bladder.

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9
Q

Medulla

A

One of the functioning parts. Contains many tubules and ducts. Has a higher na [] then cortex so there is a osmotic gradient.

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10
Q

Pelvis

A

Flat funnel cavity that collects urine into the ureter. It is called pylo when it is affected.

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11
Q

Cortex

A

Outer 1/3 of kidney. Has most of the filtration units.

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12
Q

Nephron

A

Found in cortex and medulla. Produces urine and functions to clear blood. 1 million nephron in each kidney. Ball of capillaries at the beginning (glomerulus) and then long then tube with hairpin loop. Closed at one end.

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13
Q

Peritubular Capillaries

A

Surround the nephron. Absorb water and solutes which leave renal tubules and will be taken back to the body. Provides blood supply to renal tissue.

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14
Q

Bowman’s Capsule

A

Surrounds the glomerulus. Located in the cortex. Closed at the beginning of the nephron (vascular pole) and open end is called urine pole.

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15
Q

Juxtaglomerular cells

A

Located in the afferent arterioles (turn into glomerulus). Sense pressure changes. Produce store, and excrete renin.

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16
Q

Glomerulus

A

Surrounded by bowman’s capsule. Fenstrated capillaries with incomplete BM and podocytes (support slits). Ball held together by mesangial cells with phagocytic abilities and contractile capabilities.

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17
Q

What other structures is the glomerulus similar to?

A

Choriocapillaries and RPE Cells.

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18
Q

Placing pressure on arterial flow?

A

Will decrease pressure at glomerulus and decrease flow

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19
Q

Placing pressure on efferent flow?

A

Will increase pressure at glomerulus and increase flow

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20
Q

Decreasing flow rate?

A

Will increase filtration as more particles can fall into glomerulus

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21
Q

Increasing flow rate?

A

Will decrease filtration as more particles will escape being filtrated.

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22
Q

Sympathetic effects on Nephron

A

Causes constriction of arterial flow (will cause slower blood flow and less pressure) This in turn will cause release of renin which will make angiotensin to constrict efferent arterioles. This will increase pressure. Therefore we will have greater pressure with slower rate which will allow more filtration to occur with less blood flow. These systems act to keep a constant rate of filtration. This is auto regulation. Cannot auto regulate with really high or low pressures!

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23
Q

Parasympathetic effect on Renal system

A

No significant effect! TRICK QUESTION!

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24
Q

Filtration

A

Occurs passively in the glomerlus. It has 2-3X higher pressure then other capillary beds.

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25
Q

Glomerulus selective permeability

A

Size (big cannot be filtrated)
Charge (glomerulus is neg. charged so repels other neg)
Configuration (this has a minimal effect). Higher []=more filtration.

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26
Q

What is the filtrate

A

Water, glucose, ions, amino acids, bicarbonate.

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27
Q

Reabsorption

A

Substance in the filtrate is pulled back into the body. Can be both passive or active. Reabsoprtion commonly occurs with Na+ reabsorption.

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28
Q

Modifers of reabsorption

A
  1. Concentration of molecules-the more there are the more the transporters can gather (up to a point)
  2. Flow-faster flow results in decreased ant of time to gather molecules.
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29
Q

Reabsorption of water

A

Occurs along tubules. This is major. Only 1% total urine becomes a filtrate.

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30
Q

Reabsoprtion in different parts of tubules

A

Proximal (80) Loop of hence (6) Distal (9) collecting (4). Only 1% becomes urine.

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31
Q

Secretion

A

Addition of substances to the filtrate. Occurs with unwanted components such as AB or ammonia. Can be passive (follows water) or a transporter.

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32
Q

Filtration at glomerulus

A

Filtrates water, NaCl, HCO3, K, Glucose, amino acids, creatinine, and urea. NO LARGE PROTEIN OR RBCs.

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33
Q

Reabsoprtion at proximal tubules

A

Reabsorb water, NaCl, K, HCO3, Glucose, and amino acids.
Secrete uric acid and organic acids
A diuretic here to mess with Na is ineffective as rest of system will compensate.

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34
Q

Descending loop of henle

A

Only permeable to water so reabsorption of water occurs. It is in the medulla in a hyper osmotic state

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35
Q

Ascending loop of henle

A

Inpermable to water but have active transport of NaCl and K reabsorption. Diuretics that work here will decrease NA reuptake but will cause a decrease in K as the collecting duct with trade NaCL for K when it realizes Na is low.

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36
Q

Distal Tubule

A

Secretes K and H. Reabsorbs NaCl (increased with aldosterone), H20, and Ca++ which is increased with PTH.

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37
Q

Collecting Duct

A

Has reabsorption of H20 (increased with vasopressin), and a NaCl and K transporter (increased with aldosterone) and urea (to keep osmotic gradient correct)
Excrete H20, NaCl, K, HCo3, Creatinine, and urea. Diuretics that work here are K sparing. Work by effecting aldosterone by preventing naCL reuptake and K loss.

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38
Q

What substance is not reabsorbed anywhere in the system?

A

Creatinine!

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39
Q

Why do diabetics pee a lot?

A

The body cannot reabsorb all of the glucose and it causes an osmotic drag that causes water to not be reabsorbed.

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40
Q

Macula Densa cells

A

At junction of ascending and proximal tubule and near afferent arteriole. Respond to decrease Na and CL in the filtrate (these means that the patient is dehydrated as there is less flow so more Na and Cl were able to be reabsorbed). Sends a message to juxtaglomerular cells to release renin.

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41
Q

Renin Function

A

INCREASE BP!
Kidney releases renin and liver angiotensigin which combine to angiotenosin I. ACE from lungs convert angiotenosin I to angiotenosin II. II causes vasoconstriction of arterioles, increase thirst, acts on kidney to increase Na and h20 reabsorption. Also acto on pituitary to release vasopressin. This will act on adrenal cortex to also release aldosterone. This increase Na reabsorption and water reabsorption.

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42
Q

Kidney Endocrine functions

A

Renin, erythropoiten, calcitriol, and glucose

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43
Q

Erythropoiten

A

Released by renin in response to hypoxia. Stimulates bone marrow to produce RBCs

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44
Q

Calcitriol

A

Converts vitamin D to active metabolic form Vitamine D3. D3 is important in absorbing calcium from intestines

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45
Q

Glucose function in renin

A

Still being investigated. Know that they convert lactic acid to glucose. Can target for diabetes.

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46
Q

Autocrine

A

A hormone that binds to a receptors and affects the function of the cell that produced it.

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47
Q

Kindey autocrine functions

A

Endothelins, NO, and renal prostaglandins.

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48
Q

Endothelins

A

Produced by renal system for autocrine function. Tend to cause increased vasoconstriction and increased salt and water retention resulting in increased BP.

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49
Q

Nitric Oxide

A

Autocrine in renal. Cause more water to be excreted. Helps macula dense provide feedback (altering function)

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50
Q

Renal prostaglandins

A

Autocrine in renal.. Increase blood flow to kidney by preventing vasoconstriction. Impair water reabsorption by blocking vasopressin in collecting duct, preventing water and sodium reabsorption, and prevents potassium excretion so more water is excreted.

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51
Q

Acid base balance with the kidney

A

The body keeps the pH at around 7.4. Excess hydrogen ions will combine with bicarbonate. Kidney will regenerate bicarbonate, excrete hydrogen ions when blood too acidic, and excrete bicarbonate ions when blood too basic.

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52
Q

Glomerular Filtration rate

A

Estimation. Have patient ingest inulin as filtrated by kidney and then not messed with. Measured clinically by collecting timed blood and urine samples to see how fast the substance is removed. Not popular as pt. has to stay in clinical all day

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53
Q

Creatinine Clearance Rate

A

Creatinine is produced by muscle metabolism. Filtered by kidney and not reabsorbed. Urine is collected for 24 hours with a blood draw at the end. Normal is 100 ml/min. Less then 60 is significant for kidney disease. Only use if searching for kidney disease.

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54
Q

Serum Creatinine Level

A

Depends on gender and size of individual. When value increases it indicated poor kidney function. If value doubles the kidney function has called to half its function. If it triples it has fallen to 25%. Used as a screening test!

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55
Q

BUN Test

A

Urea is an end product of protein metabolism. Generally 50% excreted and 50% reabsorbed. A slow filtration rate will result in more urea to be reabsorbed. The level will INCREASE with decreasing kidney function.

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56
Q

Azotemia

A

This is an increase in the BUN test with no symptoms.

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57
Q

Urinalysis

A

Look at content of the urine. Expect no blood, protein, or glucose. Albumin in urine is a sign of kidney involvement in DM.

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58
Q

Potassium and phosphate tests

A

Levels tend to increase in the blood with kidney failure.

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59
Q

Calcium, Ph, Bicarbonate in the serum

A

Levels tend to decrease in the blood with renal failure.

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60
Q

NGAL

A

Neutrophil gelatinase-associated lipocalin. Very favorable as it is used to detect acute renal failure (all others look at chronic) so that you can fix and allow kidney to heal itself.

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61
Q

Cystoscopy

A

Put a camera up into the bladder. Allows for visualization and biopsy of the bladder.

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62
Q

Ultrasound

A

For evaluation of tumors and structural abnormalities.

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63
Q

Radiological exams

A

CAT can detect tumors. Radiopaque iodine contrast allows visualization of urinary structures. Intravenous pyelogram allows X-ray visualization of renal tissue as dye is cleared by the kidneys.

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64
Q

Ways to describe kidney disease

A
  1. Acute or chronic (3 months or more)
  2. What systemic disease causes it (i.e. diabetic Renal failure)
  3. Type of tissue involved (i.e. glomerular kidney failure)
  4. pre/post renal or intersitial (pre= something is blocking blood flow to the kidney before the renal is encountered. Occurs with shock. intersitial=there is something wrong with the kidney itself. Post=something occurring after the kidney and causing backup)
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65
Q

Most common cause of kidney failure

A

Diabetes is number one and hypertension is number two

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66
Q

Common first signs of kidney disease

A

High blood pressure (due to renin release), swelling of the legs (less urine output), pulmonary edema (more fluid in the body and must push against that and heart must work harder), fatigue, HA, weight loss, N&V (above due to change in ions). Itching (build up of ions. Phosphate particularly causes) Have an increased tendency to bleed (don’t release erythropotient to create blood cells to stop bleeding) and have cognitive impairment.

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67
Q

Uremia

A

Occurs when the patient has clinical signs and symptoms of azotemia.

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68
Q

Chronic Kidney Disease symptoms

A
  1. Anaemia (pallar, lethargy, breathlessness. Due to decreased erythropotien and RBC)
  2. Platelet abnormability (epistaxis-bleeding, bruising. Due to decreased RBC)
  3. Skin-pigmentation (kidney normally gets rid of melanocyte stimulating hormone but doesn’t anymore) and Pruitis (itching due to ion imbalance)
  4. GI Tract-anorexia, NV, diarrhea. Due to acid base/balance and waste build up
  5. Endocrine/gonads-amenorrhea, ED, infertility. Hormones involved
  6. polyneuropathy-tingling of fingers and toes.
  7. CNS-Confusion, coma, seizures. Waste products build up
  8. CVS-Uremic pericarditis (uremia build up), hypertension, peripheral vascular disease, Heart failure (due to fluid build up)
  9. Renal-nocturia (pee at night), polyuria (need to pee a lot), salt and water retention.
  10. Renal osteodystrophy-osteomalaca, muscle weakness, bone pain, hyperparathyroidism (low calcium) osteosclerosis.
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69
Q

What are the most common and first signs and symptoms of CKD?

A

Anorexia, NV, diarrhea.

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70
Q

Acute Renal Failure

A

An abrupt decrease in renal function. Commonly due to meds, ischemia (most common. Occurs with surgery), auto-immune dis, infections. DECREASED URINE OUTPUT IS THE MOST COMMON SIGN! Remove cause and allow kidney to heal. If patient survives there is a 90% chance of full recovery.

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71
Q

Medications causing ARF

A
  1. NSAIDS-inhibits prostoglandins and stops vasodilation from occurring. Will recover with discontinuation.
  2. Hypersensitivy-not dose related. Meds bind to proteins of the kidney while cleared and indicated as foreign. Start an immune reaction. Can be type I (anaphylactic) or type IV (delayed)
  3. Toxicity-Occurs with overdose and typically comes within a week of treatment. Prognosis for recover is good.
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72
Q

Aminoglycoslides

A

Nephrotoxicity occurs in about 10% of patients

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73
Q

Radiographic contrast agents and ARF

A

Increase risk of ARF. Tell pt. to hydrate to minimize risks.

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74
Q

Acute tubular necrosis

A

A common form of intrinsic ARF (damage to the renals themselves). Response to acute ischemia or nephrotoxic insult. Decrease in GFR occurs in minutes to days. Damage of tubular epithelial cells decreases ion transport and cells can slough off and block tubules and can alter the medulla and increase intratubular pressure and cause collapse. Insult damages vasculature and results in increased endothelial with decreased NO and prostoglandins so results in vasoconstriction. Causes reduced volume of urine, increased fluid in body and increased waste products in the blood.

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75
Q

Malignant Hypertension

A

An example of intrinsic ARF. Symptoms-HAs possibly occipital, NV, Visual scotoma and spots. Char=diastolic BP >120. ONH edema, encephalopathy, CV abnormalities, renal failure (causing the increased HTN). A vicious cycle occurs where there is damage to kidney that results in increased permeability of small vessels, that results in fibrosis of vessels to stop leaks, that leads to ischemia to kidney, that rsults in renin release and more vasoconstriction.

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76
Q

Glomerular disease

A

Affects the glomerulus. Included nephrotic syndrome, nephritic syndrome, and mixed: membranoproliferative glomerulonephritis

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77
Q

Nephrotic syndrome

A

Have a derangement of capillary walls so they are more leaky. Have massive proteinuria (seen as bubbly pee), hypoalbuminemia (as it is escaping in the pee. Causes production of all plasma proteins including lipoproteins) and has hyperlipiduria and hyperlipedimia. There is also an impaired breakdown of lipoproteins so there is an increased risk of thromboembolism. Will have generalized edema (eyelids often first. Decreased albumin in blood shifts balance. Pitting edema. and decreased blood to kidneys causes release of renin (HTN possible but not universal. Not expected as fluid is in tissue and not the blood vessels so there is less fluid in blood vessels)*** NOTE: no oligouria like in nephritic.

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78
Q

Common causes of nephrotic syndrome

A

Diabetes and HTN (most common), lupus, NSAID induced, membranoproliferative glomerulonephritis, idiopathic.

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79
Q

TX for nephrotic syndrome

A

Try to get control over protein loss. ACE inhibitors or Angtiotensogen receptor blocker will decrease protein in urine by decreasing filtration rate to improve charge and size selectivity of glomerular BM. Use diuretics (especially loop to remove fluid). Fluid and sodium restrictions, Thrombo-prophylaxis for first 6th months to stop clot development. Can use immune suppression in children and some adults (90% respond to corticosteroids but proteinuria recurs in more then 66%)

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80
Q

Acute glomerulonephritis AKA acute nephritic syndrome

A

Acute inflammation of glomeruli with hematuria* (blood vessels of tubules are leaking). One of the first manifestations may be oliguria* (reduction in urine output). Mild edema usually on the eyelids and face first. Retention of salt causes fluid retention and HTN* (fluid retention in vasculature unlike nephrotic syndrome)

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81
Q

Causes of nephritic syndrome

A
  1. prior streptococcal infection-occurs 12-14 days after infection. Inflammation from ag-ab rxn. More common in kids, summer and autumn. Post strep in northern US and post impetigo in southern US.
  2. staphylcocci and gram neg bacteria: subacute bacterial endocarditis (valves aren’t working right and bacteria can grow here), dental abscess, and shunt infections
  3. Lupus-consider if no prior infections
  4. Can be idiopathic
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82
Q

TX for nephritic syndrome

A

Salt restrictions, diuretics and other HTN meds. Complete recovery in 90-95%. Can take 1-2 years for some.

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83
Q

Nephrotic vs. nephritic

A

Nephrotic has loss of protein with hyperalbuminurea and hyperlipidema and hyperlipidurea (increased risk of stroke). There is pitting edema but normally no increased HTN as in tissue and not vessels. Treat with loop diuretics, ACE inhibitor or ARB (decrease flow and allow more correct filtration), thrombi prophylaxis, and immunosuppresents.
Nephritic syndrome has hematouria, oligouria, and HTN (fluid in vasculature) Treat with loop diuretics and HTN, decrease salt and fluid.

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84
Q

Membranoproliferative glomerulonephritis AKA dense deposit disease

A

Immune damage to capillaries and mesangium. Three subtypes of unknown cause. Can cause HTN and signs of nephrotic syndrome (mix of nephrotic and nephritic)

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85
Q

Type II Membranoproliferative glomerulonephritis

A

Associated with bilateral central clustered drusen. Often found in tens. Initially VA and VF unchanged. Longer term have poor night vision, Subretinal neovascularization macular, macular detachment, central serious retinopathy, and retinal atrophy.

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86
Q

Tubulointerstitial nephropathy

A

A group of inflammatory kidney diseases that primarily involves the intersitium and tubules. Spares glomerulus and renal vessels. Can be acute or chronic. often caused by pyelonephritis (bacterial infections of renal pelvis). If non-infections called interstitial nephritis (drugs and metabolic disorders or physical injuries)

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87
Q

TINU (acute idiopathic tubulointeristial nephritis and uveitis)

A

Occurs in females 10-33 (bimodal 10-15 and 28-33). Bilateral uveitis in majority (77). Ocular systems occur first in 33% and are often recurrent. Conj injections, fine KP, iridocyclitis. Fever, weight loss, fatigue (50). Use oral corticosteroids to treat uveitis.

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88
Q

Acute pyelonephritis

A

Inflammation of the kidney and renal pelvis. Almost always bacteria getting to the kidney by the bladder and ureters. Almost exclusively in women (common in pregnancy). Will have fever, dysuria (painful urination), back pain, and pyuria (pus in urine). usually very responsive to AB.

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89
Q

Chronic pyelonephritis

A

slowly progressing disease that kills the kidneys. Often only signs are not feeling well so diagnosed late. usually some pyuria. Primary underlying disorders is frequent UTI rom obstruction, vesicoureteric reflex (pressure on glomerulus as there is a blockage that causes urine to travel backwards), or diabetic nephropathy. Many will wind up on renal dialysis.

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90
Q

Diabetic nephropathy

A

Most common cause of ESRD in US. Direct result of metabolic changes in DM. (good blood sugar level is protective). Have microalbuminuria and proteinuria. ACE inhibitors and ARB reduce protein in urine. Nephrotic syndrome and azotemia develop 3-5 years after proteinuria. ESRD 1-5 yrs after that. Accelerated decline with HTN, infection, nephrotoxins.

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91
Q

Diabetic Neuropathy Pathology

A

Occurs due to glomerulus membrane thickening, renal atherosclerosis (affects both afferent and efferent arterioles and changes blood flow to kidneys), and pyelonephritis (increased suspectiblity to infection)

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92
Q

Fabry Disease

A

Error of glycosphingolipid metabolism due to enzyme (alpha-galactosidase A) defect. X-linked recessive but carrier can show some symptoms (more common M) Difficult to diagnose due to variable signs and symptoms (most caused by build up of lipids in tissues).

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93
Q

Fabry Disease Symptoms

A

Children will have burning sensation in hands, raised rash on butts, decreased ability to sweat, corneal whorl or verticillata (present in over 90%. Deposit in bowman’s). Some other ocular signs are conj vessel tortuosity and sacular dilation, retinal venous dilation with hemorrhages possible or a spoke like cataract.

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94
Q

Systemic problems with fabry

A

Renal failure is common (proteinuria, azotemia, uremia. Due to glycolipid deposition and damage to renal vessels. 50% affected by age 35 if treated). Cardiovascular disease, cerebrovascular disease, GI disfunction.

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95
Q

Testing for fabrys

A 
Enzyme assay (measure amount of alpha-GAL enzyme activity)
Genetic testing (evaluate for mutation)
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96
Q

Treatment for Fabry

A

Enzyme replacement with agalsidase beta given IV. Recombinate agent given every 2 weeks, protects kidney function.

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97
Q

Nephrolithiasis (urolithiasis)

A

Formation of calculus in the collecting system. Travels and gets stuck in ureters. Blocks urine flow. Can occur with meds (zcetazolaminde), dehydration, or gout. Made of calcium, mg, uric acid or cysteine. M more commonly have symptoms. 20-45. Hematuria and severe pain!

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98
Q

Nephrolithiasis treatment and diagnosis.

A

Diagnosed with a CAT scan. Treat with pain meds (allow to pass). Meds to allow spontaneous passage (Alpha-adrenergic blockers and calcium channel blockers). Dietary modifications to stop another. AB while allowing to pass. Shockwave lithotripsy (breaks up the stone if it cannot pass) Surgery in intense cases.

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99
Q

Renal Cell Carcinoma

A

90% malignant tumors of the kidney. M>F. Greater frequency in cigarette smokers. Associated with von Hippel-Lindau Disease (bleeding in the eye). Prescent with painless hematuria. Classic triad is Hematuria, dull flank pain, palpable flank mass (only 20% have this). Can also have a long standing fever, elevated sedimentation rate (longer for red blood cells to settle) and systemic signs of cancer. Develops form the proximal tubules and is highly vascular

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100
Q

Renal Cell Carcinoma TX

A

Usually treated by surgical removal of the kidney (if before metastasize). Today experimenting with percutaneous cryoablation (lower temperature of kidney). Resistant to chemo. Anti-VEGF and anti-PDGRF are having some success. Immune modulators are also being explored (aldesleukin). 5 year survival rate of 70% if no metastasis.

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101
Q

Wilms’ Tumor

A

Second most common renal malignancy. 3rd most common organ tumor in children <10. Can grow really big and result in ab distention. High incidence in children with aniridia. Treat with radiotherapy, nephrectomy and chemotherapy. 90% survive for two years.

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102
Q

Treatment for CRF

A
  1. remove cause if known
  2. Treatment of HTN (decrease progression)
  3. Treatment of secondary manifestations (Heart disease, edema, anemia)
  4. Restriction of dietary protein until on dialysis
  5. Avoid toxic meds
  6. short or long term dialysis
  7. Renal transplantation
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103
Q

Anti-HTN drugs

A
  1. Diuretics-pull water out. work best in the beginning as kidney will adapt
  2. Beta-blockers-Lower HR and Relaxes smooth muscle
  3. Calcium channel blockers-relaxes smooth muscle.
  4. ACEi*
  5. Antiotensin II antagonist (ARB)*
  6. Renin inhibitors
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104
Q

What drugs are used with diabetics to try and decrease protein in the urine

A
  1. ACEi
  2. ARB
  3. Renin inhibitors.
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105
Q

Diuretics

A

Decrease sodium reabsorption so increase urine output and initially reduce blood volume. Blood volume may return to normal if kidney is working. Usefull in patients with HTN due to renal disease.

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106
Q

Hydrochlorothiazide

A

Thiazide. Works on distal tubule.

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107
Q

Chlorthalidone

A

Thiazide. Works on distal tubule.

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108
Q

Bumetanide

A

Loop diuretic. Works on ascending.

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109
Q

Furosemide

A

Loop diuretic. Works on ascending

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110
Q

Spironolactone

A

Potassium sparing diuretic. Works on collecting duct.

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111
Q

Triamterene

A

Potassium sparing diuretic. Works on collecting duct.

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112
Q

Acetazolamide

A

Carbonic anhydrase inhibitor. Works on the proximal tubule to stop absorption of bicarbonates. Used for glaucoma or disc edema. Can cause renal stones

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113
Q

Mannitol

A

osmotic diuretics. Used in glaucoma

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114
Q

Urea

A

Osmotic diuretics. used in glaucoma

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115
Q

Isosorbide

A

Osmotic diuretics. used in glaucoma.

116
Q

When should you start dialysis

A
  1. Current criteria is GFR: 15 ml/min for diabetics and <10 for nondiabetis. But studies suggest this might be too soon
  2. Recent studies: Wait for uremia symptoms namely neuropathy or pericarditis before considering.
117
Q

Hemodialysis

A

Most common dialysis. Blood circulated out of the body into articifical kidney machine. Another fluid pumped through machine in opposite direction with semipermeable membrane. Allows diffusion of ions and low mol. weight substance from blood to dialysate. Blood circulated back into the body. Takes a long time commitment and has low creatinine clearance. Must be on low protein diet. Risks of anemia, pulmonary edema, ionic dysfunction, infection, heart dysfunction. Greater visual impairment on dialysis.

118
Q

Peritoneal Dialysis

A

Patient has indwelling catheter in peritoneal cavity. Instal 1-3L of dialysate into peritoneal cavity. Peritoneum acts as a semipermeable membrane and waste moved to bag. Dialystate removed and more added. In continuous ambulatory peritoneal dialysis (CAPD) fluid is constantly in peritoneum.

119
Q

Advantages and disadvantages of peritoneal dialysis over hemidialysis

A

Advantages: less time, less dietary restructure, more consistent filtration, residual kidney fx retained longer. Cheaper
Disadvantages: pt. must be knowledgeable and peritonitis.

120
Q

Renal transplantation

A

Best treatment for ESRD. Have improved quality of life. Live donation is best. Matched for HLA type, blood, and gender (Y is foreign to F). Must be on immunosupression for life!

121
Q

Renal transplantation immunosuppresion

A
  1. Corticosteroid-prednisone
  2. Calcinurin inhibitor-decrease IL2 production by T cells to stop self replication (cyclosporine or tacrlimus*)
  3. Anti-metabolite: decrease lymphocyte proliferation and activation (Azathioprine which is a DMARD or mycophenolate*)
    85% pt discarged on drugs
122
Q

Cyclosporine

A

Calcineurin inhibior (decreased IL2 production by T cells to stop self replication). Used with renal transplant but not preferred drug.

123
Q

tacrolimus

A

Calcineurin inhibitor (decreased IL2 to stop T Cell replication). Preferred drug for renal transplant

124
Q

Azathioprine

A

Anti-metabolite. DMARD. Used for renal transplant but not preferred

125
Q

Mycophenolate

A

Anti-metabolite. Used with renal transplant. Preferred.

126
Q

Prednisone

A

Can be used for immunosuppresent but not as popular due to side effects (cataracts, glaucoma, papilledema)

127
Q

Transplantation Complications

A
  1. immunosuppresive disorders
  2. Secondary HTN due to prednisone and native kidney renin production
  3. Infections such as UTI, hepatitis
  4. Have an increased risk of malignancy. Skin cancer, Kapasi’s sarcoma (decreased with rapamune-anti-metabolite) Ocular squamous cell carcinoma.
128
Q

Prescribing medication for renal compromised pt

A
  1. Avoid medicine toxic to the kidneys-especialy aminoglycoside and tetracycline (except doxycline)
  2. Adjust amt. of medication given based on CrCL. Can decrease dose or increase interval. Can also look in sources.
129
Q

Dose formula

A

Dose=(pt CrCl/normal CrCl) X normal dose

130
Q

Dosing interval

A

Interval=(normal CrCl/pt crcl) X normal interval (in hours)

131
Q

CVD

A

Very prevalent and number one killer in US

132
Q

Ocular symptoms of CVD

A

Retinal a. and v. occlusion, macroaneurysm, other vessel changes. Transient ischemic attacks. Retinopathy increases risk of Heart disease 2-6X. Other ischemic syndrome.

133
Q

Disease with ocular and heart affects

A

Diabetes, HTN, atherosclerosis, valve disorder, marfan syndrome.

134
Q

Why do we care about cardiovascular dz as optometrist?

A

Some procedures we do require prophylactic AB prior with valve disease.

135
Q

Which side of the heart is stronger?

A

The left side. It must push oxygenated blood to the entire body

136
Q

Which side of the heart is weaker?

A

The right side. It must only push blood to the lungs.

137
Q

The cardiovascular system is a ______ system

A

Closed. Something happening on the left side of the heart will eventually affect the right side!

138
Q

V. vs A.

A

smaller veins do not have musculature. Arteries tend to be smaller then veins. A have a smaller lumen due to muscles. Veins will have valves.

139
Q

Endothelium

A

Lines the entire vascular system. Involved with blood tissue interchange, control of clotting, vessel repair, reg. of inflam, modulation of blood flow, reg of cell growth, oxidation of low-density lipoprotein.

140
Q

Tricuspid valve

A

Between R atrium and ventrical

141
Q

Plumonic valve

A

Between R ventricle and pulmonary a.

142
Q

Mitral valve/bicuspid

A

Between L atrium and ventrical

143
Q

Aortic valve

A

Between L ventricle and aorta.

144
Q

Valves action

A

Block blood flow by a passive process.

145
Q

Left atrium appendages

A

And outpoutching though to provide pressure release area. Blood can get stuck here in a poor functioning heart.

146
Q

Coronary arteries

A

Supply oxygenated blood to the heart tissue. There are two main arteries (l and R coronary a.) Blockage can lead to severe heart disease, MI, and death

147
Q

Rank most commonly blocked coronary arteries

A
  1. Left coronary a
  2. Right coronary a
  3. left anterior descending.
148
Q

Heart Rate

A

Controlled by SA node. Normal rate is 60-100. Want a lower rate when resting.

149
Q

Tachycardia

A

HR greater then 100

150
Q

Bradycardia

A

HR less then 60

151
Q

SA node

A

In the right atrium wall. Depolarizes spontaneously and keep HR at 60-100.

152
Q

Systole

A

Contraction. Occurs when ventricle contract and pump blood to the pulmonary a. and aorta. Tricuspid and mitral valves close at the beginning to prevent back up of blood into the atria. This is the first heart sound heard. When eMpTying-tricspid and mitral close.

153
Q

Diastole

A

Dilation. Relaxation and filling of the heart. Ventrical walls relax and blood flows into the heart from vena cava and pulmonary veins. Open tricuspid and mitral valves. Pulmonary and aortic valves close at end of systole and beginning of diastole (second heart sound herds). Ends after atrial walls contract and force blood into the ventricles.

154
Q

Preload

A

Amt. of blood in the ventricles after diastole. Due to venous return. Frank-starling=more fill results in more contraction.

155
Q

Afterload

A

Force against with the ventricles must contract to eject blood. Main portion is arterial pressure. Other factors include thickness of blood, elasticity of the vessels, etc.

156
Q

Contractility (inotropy)

A

Force of ventricular contraction ind. of loading conditions. (contractility and pre-load can be related but contractility is an innate ability of the fibers to change shape). Influcnced by calcium and B-1 system. Medications are a major modifier (i.e. beta blockers)

157
Q

Cardiac output

A

Amt of blood ejected by the heart each minute. Depends on contractility and rate. Normal is 5-6L/min.

158
Q

Cardiac Index

A

Cardiac output divided by body surface area. Makes it so you can compare people that are of different sizes accurately. Normal is 2.6-4.2L/Min/m2

159
Q

Heart conduction

A

Electrical impulses start in the SA node and passes to the AV node and to the atriums causing them to contract. The AV node stalls and then sends signals along the bundle of his which divides to L and R. These become purkinje fibers which cause the ventricle walls to contract.

160
Q

Redundancy in the heart conduction

A

If SA node fails the AV node can take over but at a lower rate (40-60) and if AV nodes fails the bundle of his can take over (even at a slower pace)

161
Q

syncitium

A

A group of cells that have all their membranes fused together so when one fires they all fire. This is what the cells in the atrium and ventricles are like.

162
Q

Sympathetic regulation of the Heart

A

Cause an increased heart rate through beta-1 receptors in SA and AV nodes and by shortening AV delay. Also causes increased contractility of the heart with calcium. Intervates the atria and ventricles. The end result is an increase in Cardiac output.

163
Q

Parasympathetic regulation of the heart

A

Decrease HR through SA and AV node and increases AV delay. Innervates atria by vagus n. No ventricle enervation. Slight decrease in contractility. Overall decreased Cardiac output.

164
Q

Resting membrane potential of general cells

A

Negative. Due to Na/K pump of 3/2 and the cell being more permeable to leaking out K then sodium leaks in.

165
Q

General action potential

A

Stimulus causes a neutral charge. The Na gates open and Na rushes in and we have depolarization. Na gates then close and K channels open. K rushes out quickly and hyperpolarization occurs and gates close. The pump and permeability re-establishes normal.

166
Q

Cardiac Node AP

A

Self excitatory as cells are naturally leaky to sodium and calcium. Depolarization occurs once enough plus gets in. There is a fast initial depolarization due to Na coming in. Ca channels also triggered to open. Ca comes in as slower response. Ca channels are triggered to close. This causes the depolarization to last even as K starts to leave. Finally after both ca and K channels close the cell repolarizes.

167
Q

Atrial and ventricle muscles

A

Striated muscle with thick myosin and thin actin filaments with regulatory proteins tropomyosin and troponin. The cells are smaller then skeletal muscle. Cell membranes are fused with each other and allows low resistance for electrical activity and easy flow of ions. (i.e. they are a syncytia)

168
Q

Ca effect on cardiac muscle

A

Calcium increases the plateau but also increases contractility. As Ca enters the cell it causes release of more Ca from SR and mitochondria. Increased concentration of unbound Ca results in increased contraction.. If Ca stayed in the cell it would remain contracted.

169
Q

Removal of Ca

A

Occurs through the sodium-calcium exchange. Sodium put into the cell through Ca channel and Ca taken out of the cell by the Ca channel. Calcium is re-uptaken into the SR and mitochondria.

170
Q

Meds interfering with sodium-potassium pump

A

EX: Digitalis. Interfere with the sodium potassium pump. Cause slower conduction through the AV node and slow tachycardia and fibrillations. Increases contraction by increasing intracellular Ca. Have visual SE of blurry vision, alteration in color.

171
Q

Calcium channel blocker

A

Verpamil. Delay influx of calcium into smooth muscle of vascular system (vasodilation). Decreases heart contractility. Delays removal of calcium from pacemaker cells (slows heart rate by interfering with SA and AV node)

172
Q

Beta Blockers

A

Block the action of epinephrine. Cause decreased heart rate and less force (less contractility) and slows conduction time. Not to be used with severe heart block as it will make block worse.

173
Q

Serum Enzyme Test

A

Designed to look for signs that the Heart muscle is dieing (usually done after MI). Increased levels that go down again indicate a MI has occurred. Usually blood is drawn many times. There are three different things that you can look for (creatine phosphokinase, lactate dehydrogenase, tropnin). Which test you do depends on when the pt. comes to the emergence room.

174
Q

Creatine phosphokinase

A

increased in 2-6 hours, peak in 12-24 hours and gone in 3 days.

175
Q

Lactate Dehydrogenase.

A

Increased 24-72, peak 2-5 days. Normal in 14 days.

176
Q

Troponin I

A

Increase in 4-6 hours, peak 10-24 hours. Normal in 10-15 days. The most selective for heart muscle so we will often do.

177
Q

Electrocardiogram

A

Graphical displays of electrical signals generated by the heart. Shows 5 waves. P=atrial depolarization QRS=ventrical depolarization T=ventrical depolarization PR interval=measure of AV conduction time.

178
Q

The stress test

A

AKA Excersice tolerance test (ETT)
Determines heart response to exertion. An ECG, blood pressure, and pulse are measured during exercise or stress. Chang in ECG during increased workload indicated prescense and severity of ischemia.

179
Q

Angiography

A

Inject dye into the blood stream and heart. X-ray films are taken to evaluate blood flow in heart and large blood vessels from heart.

180
Q

Coronary Calcium Scan

A

CT to evaluate calcium build-up in coronary arteries. Used for those with risks but no symptoms. Scored form 0-500. Those >100 are at a great risk of coronary a. disease.

181
Q

Ultrasonography

A

During electrocardiography, ultrasound transmitted into the chest. Shows the structure and movement of the heart. Doppler is a special form of this for BVs.

182
Q

MUGA Scan

A

Radioactive test which studies the motion of the left ventricle wall. Measures ventricles ability to eject blood and test function of the heart and cardiac output. Can see volume with diastole and systole.

183
Q

Stress Thallium

A

AKA DIP-Thal. Thallium 201: radioactive isotope injected into the veins and taken up by myocardial tissues. Concentration of thallium measured by scanning. Infarcted or scared heart tissue does not take up any isotope. This is known as a cold spot. DIP is a medication that puts stress on the heart by causing vas dilation of healthy but not of unhealthy.

184
Q

Symptoms of Arrhythmias

A
  1. palpitations
  2. lightheadedness
  3. syncope-fainting
  4. anxiety
  5. diziness
  6. chest discomfort
  7. neck discomfort
  8. dyspnea
  9. weakness.
185
Q

Asymptomatic arrhythmia

A

Urgent treatment NOT needed! Have them see PCP but not immediately!.

186
Q

Diagnosing arrhythmia

A
  1. history
  2. clinical exam
  3. EKG: holter monitor or event monitor (only push when event)
  4. Echocardiogram-analyze and look for any structural changes.
187
Q

Type of arrhythmias

A
  1. Bradyarrhythmia vs. tachyarrhythmia
  2. Supraventrical vs. ventrical
  3. Regular vs. irregular
188
Q

Tachyarrhythmia vs bradyarrhytmia

A

Too fast or too slow heart beat.

189
Q

Supraventricular (atrial) vs ventrical

A

Supraventrical: problem with nodes or atrial
Ventrical: problem with nodes.
Ventrical is more concern as atrial has no large effect on CO

190
Q

Regular irregular

A

Beating is not normal but can tell when it is coming Can be too fast or too slow

191
Q

Irregular irregularity

A

Beating is not normal and you can’t tell when it is coming.

192
Q

Supraventricular Tachycardias

A
  1. sinus tachycardia
  2. Atrial fibrilation
  3. Paroxysomal supraventricular tachycardia
    a. Atrioventricular nodal re-entry tachycardias
    b. wolff-parkinson-white syndrome
193
Q

Sinus tachycardia

A

Increased rate of SA node. SA node is still in control but is firing at a faster rate. Common causes are normal exercise, etc. Can also be from anemia (need more oxygen and feedback loop taken) or hyperthyroidism (everything in overdrive) or Heart failure (receptors tell heart to spread up with reduced CO).
TX: Treat underlying disease process or treat with agents to decrease SA node (Beta blockers or calcium antagonist)

194
Q

Atrial Fibrillation

A

Most common sustained rhythm disturbance. Irregularly irregular arrhythmia. Atria depolarized by signals that arise near pulmonary arteries (unsure what). 300-600 bpm with no pattern Ventrical contract at irregular rate of 120-170 (AV node slightly stalls)

195
Q

Atrial Fibrillation causes

A

Three classic causes: rheumatic Heart disease, excessive alcohol, thyrotoxicosis
Most common causes: HTN and HF
Other: Stress, smoking, familiar.

196
Q

What are people with Atrial fibrillation at a greater risk for?

A

Ischemic stroke (severe), embolization, dementia even w/o a stroke.

197
Q

TX for atrial fibrilation

A

Treatments to resolve any underlying cause as well as…

  1. Meds to slow ventricular contractions- beta blockers and CCBs
  2. Use Na/K ATP pump to prolong action potential- Amiodarone, Dronedarone
  3. Radiofrequency ablation-kill cells near pulmonary vessels.
  4. May need electrical cardioversion if bad enough.
  5. Anticoagulants to prevent embolization
198
Q

Warfarin

A

Prevent embolization. Vitamin K antagonist. Can add vitamin K if overdose occurs. use with Atrial fibrillation.

199
Q

Dabigatran

A

Anti-thrombin. Prevent embolization. use with atrial fibrillation. No antidotes

200
Q

Apixaban

A

Anti-throbmin. use with atrial fibrillation. Factor Xa inhibitor. No antidote

201
Q

Rivaroxaban

A

Anti-thrombin. use with atrial fibrillation. Factor xa inhibitor. No antidote.

202
Q

Watchman

A

Left atrial apendage closure device.

203
Q

Ocular adverse reaction to amiodarone

A

Na/K ATPase inhibitor. Prolong AP. 90% develop corneal deposits that looks like fairy disease. Disc edema, optic neuritis (rare but permanent) and lens opacities. Pt. need a baseline exam, then q6m and should come back with disturbances.

204
Q

Ocular adverse rxn to Warfarin

A

Major risk of bleeding: subconj. hemorrhage, spontaneous hyphen, retinal or vitreous hemorrhage, cerebral hemorrhage. Send pt for prothrombin time and INR. Consult with PCP and cardiologist.

205
Q

AV nodal re-entry tachycardia

A

Occurs in pt. with otherwise normal hearts. More common in women. Occurs in pt. that have two functionally different paths through the AV node. Second path is slower to depolarize and but has a shorter refractory period. Impulse can travel through each and cause AV node to fire by reentry. HR of 150-200.

206
Q

AVNRT Tx

A

Increase vagal tone (para) to SA node to intercepts and stop re-entry

  1. Mechanical maneuvers: Carotid sinus massage, valsalva maneuver, head immersion in cold water
  2. Med treatment: IV administration of drugs to slow Heart: Adenosine
207
Q

AVNRT prevention

A

Long acting beta blocker, calcium channel blockers, and digitals (na/k) The above slows the HR and stops an extra beat from occurring. Can also do radio frequency ablation of slow pathway of AV node.

208
Q

Wolff-Parkinson-White Syndrome

A

Accessory connection between the atria and ventricles that allows impulses to move quickly in both directions. Can be random or inherited. M>F. More prone than AVNRT to atrial fibrillation which can lead to ventricular fibrillation. Can be treated with meds or ablation.

209
Q

Types of ventricular tachyarrhythmias

A
  1. Premature ventricular beats
  2. Sustained ventricular tachycardia (life threatening)
  3. Ventricular fibrillation (life threatening)
210
Q

Premature Ventricular Contraction (PVC)

A

Extra heart beat arise directly from the ventricles. Usually has no effect on SA node so next sinus beat occurs as normal. Increased frequency with age, infection, stress, caffeine, alcohol. No long term effects or Tx unless caused by HTN.

211
Q

Sustained ventricular tachycardia

A

Longer then 30 seconds. Occurs paroxysmally (comes and goes for no reason). Often in pt. with underlying structural heart disease. Cardiac relaxation is impaired. Results in poor CO. Usually requires direct current cardioversion. (paddles)

212
Q

Ventricular Fibrillation

A

Very rapid and irregular HR. No order to contraction of the ventricles. Results in no CO and causes death without CPR or electrical defibrillation. Survivors at a high risk for sudden cardiac death-implanted cardiovert-defibrillators are used to treat.

213
Q

Bradycardia

A

Result from inadequate SA node activity or blocked conduction.

214
Q

Sinus bradycardia

A

may be a response to hypothyroidism, drugs, athletes. If extreme may cause symptoms. Treat with atropine to increase sinus rate or treat with pacemaker implantation.

215
Q

AV Block

A

Some of the impulses from the SA node are not conducted to the AV node. Block can occur anywhere in the system. Usually at the level of the AV node or purkinje fibers. Incidence increases with age and can occur with some medications.

216
Q

First Degree AV block

A

Prolongation of AV conduction time but signal does get to the ventricles. Results in bradycardia. Seldom has symptoms or needs treatment but must be careful of beta blockers.

217
Q

Second Degree AV Block

A

Intermittent failure of the impulse to get from atrium to the ventricles. May need a pacemaker.

218
Q

Complete or third degree AV Block

A

No atrial impulses reach the ventricles. AV node can take over job of pacemaker or ventricles can start to spontaneously fire. Severe bradycardia can occur (15-40 bpm). Needs pacemaker implantation.

219
Q

Why is it important to check someones pulse before putting them on drugs?

A

If they have a block you can put them into a higher block.

220
Q

HTN ocular assocaition

A

Increases risk for hypertensive retinopathy, retinal artery emboli, anterior ischemic optic neuropathy, and retinal v. and a. occlusion. May increase risk for diabetic retinopathy and ARMD.

221
Q

HTN Epidemiology

A

1/3 of US population has high blood pressure. It is increasing! Increases risk for stroke, CVD. Variations are also important.

222
Q

What is the second most common cause of preventable deaths in the US?

A

HTN.

223
Q

HTN Risk factors

A

Obestity, Family, Dyslipidemia (high chop), Renal disease, Male gender or post meno women, increased age, alcohol abuse, sedentary life, cigarette, DM, meds, lack of sleep, low vitamin D.

224
Q

BP

A

Varies during the day for patient. Average of 2 or more BP readings on each of two or more office visits or 24 hours BP monitor.

225
Q

Normal Systolic

A

<120

226
Q

Pre-HTN systolic

A

120-139

227
Q

Stage 1 HTN systolic

A

140-159

228
Q

Stage 2 HTN Systolic

A

Greater then or equal to 160

229
Q

HTN urgency systolic

A

Greater then 180

230
Q

HTN emergency

A

Urgent BP with organ damage

231
Q

Normal Diastolic

A

Less then 80

232
Q

Pre-HTN diastolic

A

80-89

233
Q

HTN Stage 1 diastolic

A

90-99

234
Q

HTN stage 2 diastolic

A

greater then 100

235
Q

Hypertensive urgency diastolic

A

Greater then 110

236
Q

Normal BP

A

Recheck in 2 years

237
Q

Pre-htn BP

A

Recheck in 1 year. Discuss lifestyle modification

238
Q

HTN 1 BP

A

Confirm within 2 months

239
Q

HTN 2 BP

A

Refer to PCP within one month. Want to do 2 readings before refer

240
Q

HTN Urgency

A

Refer to PCP within 1 week. Don’t do two readings

241
Q

Systolic greaten then 220 or diastolic greater then 120

A

Refer within 24-48 hours if no end organ effects. Refer within a few hours if end organ effects.

242
Q

Cardiovascular End organ effects

A

Atherosclerosis, Coranary artery disease, heart failure, left ventricular hypertrophy, MI, unstable angina, aneurysm

243
Q

Brain End organ effects

A

Hemmorrhagic stroke, alzheimer’s disease, confusion

244
Q

CKD End organ disease

A

Atherosclerosis of renal arteries leads to ischemia

245
Q

End organ effects in lungs

A

Pulmonary edema

246
Q

Eye end organ effects

A

Retinopathy, swelling of ONH

247
Q

Evaluation of BP for 3 to 18

A
  1. Use CDC growth chart to find child’s height percentile
  2. Use the genera appropriate BP chart and find BP percentile.
  3. Determine classification based on percentile.
248
Q

Classification for <18 year olds with BP

A

Normal: 5 mm about the 99th percentile

249
Q

Management for child with normal HTN

A

Recheck at next exam and encourage healthy activity

250
Q

Management for childen with pre-HTN

A

Recheck in 6 months. Weight management counseling if overweight.

251
Q

Management for kids with HNT 1

A

Recheck in 1-2 weeks. If increased 2 or more times refers within 1 month. Weight mgmt. counseling. Only initiate therapy if compelling reasons

252
Q

Mgmt for kids with HTN 2

A

Refer within 1 week or immediately if symptoms. Weight mgmt. counseling. Initiate therapy.

253
Q

Consideration in HTN therapy

A

Untreated HTN reduces life expectancy by 10-20 years. Reduces cardiovascular risk, stroke, MI, HF.

254
Q

JNC standards

A
  1. 60 <140/90 (used to be under tighter control)

5. Says nothing about BP for those with target organ damage.

255
Q

What factors influence BP?

A
  1. Peripheral resistance-influcned by tunica media in arterioles. (vessel size-symp system increases vasoconstriction. particularly Alpha 1. Vessel elasticity. Blood viscosity.
  2. CO: Blood vol (symp. system increases renin by kidneys. B1) HR: sympathetic system increases (B1)
    An increase in PR or CO will increase BP.
256
Q

Baroreceptors

A

Feedback for HTN. Detect too much blood and they are stretched and make mechanisms to diminish blood volume

257
Q

Juxtaglomerular cells

A

Feedback for HTN. Increase the blood pressure.

258
Q

Serum Osmolarity

A

Feedback for HTN. Looks at osmolarity of the blood (NOT URINE LIKE MACULA DENSA) as an osmolarity increases it is deemed dehydration.

259
Q

Increased Blood CO2 and H+

A

Feedback for HTN. Body interprets as inadequate tissue perfusion. Increases sympathetic brain stem activity. Want the heart to pump more.

260
Q

Primary HTN

A

95% of adults have it. No known cause. Enviormental and genetic factors contribute (intake of salt, obesity and lack of exercise, abnormal peripheral resistance). Are staring to find genes associated (abnormalities with renin-angiotensin-aldosterone and impaired natriuresis-ability to move salt into the urine)

261
Q

Secondary HTN

A

Has a known cause. Can be due too…

  1. CKD (most imp. in those less then 20)
  2. Endo dz (tumors in adrenal or pit. Thyroid disease)
  3. Sleep apnea or deprivation
  4. Medications-contraceptives, cold remedies or appetite sup presents. NSAIDS.
    * *Must look for one of these causes in those less then 20
262
Q

Lifestyle Mgmt for HTN

A
  1. pt ed
  2. smoking cessation
  3. Sodium restirction to less then 2.3 g/d
  4. Maintain 90 mmol/d of potassium
  5. maintain adequate calcium, mg, and vit D
  6. Weight reduction and exercise
  7. DASH diet
  8. Limit alcohol intake
  9. Dark chocolate
  10. Laughter-decrease sump. activity and dilate bv
263
Q

First line drugs for HTN

A

Thiazide, ACEi, ARB, CCB

264
Q

Thiazide

A

Used for HTN. Decrease Na reabsorption and Ca secretion in distal convoluted tubule. (short term) Increases vasodilation (long term). Mainstay of Tx in HTN. May cause a transient increase in myopia.

265
Q

Loop

A

Used for HTN. Decrease ion absorption in ascending loop of hence. Most effacious with rapid onset.

266
Q

Potassium sparing/aldosterone antagonsit

A

Used for HTN. Decrease Na reabsorption and K secretion in collecting duct. Bind with aldosterone receptors sites to prevent aldosterone form working.

267
Q

Drugs selective for Beta 1 blocking

A

Primary decrease symp outflow and cardiac outflow by decreasing HR and contractility. Decreaes renine release. Do not use topical B-blocker if pt. on systemic. May lower IOP. Often given BIP and may cause decreased ONH perfusion at night. Can cause visual hallucinations at high doses

268
Q

Non-Selective Beta Blockers

A

Decreases sump. which decreases cardiac output by decreases HR and contractility. Decreases renin release. Don’t use topical beta blocker if oral is taken. Can decrease IOP. When taken at night can decrease perfusion to ONH. Can cause visual hallucinations at high doses. Concern of increased stroke and MI.

269
Q

Alpha and Beta Blockers

A

Decrease sump act–>decreased CO–>decrease HR and Contractility. Reduces renin release. Also relaxes smooth muscle. Don’t give topical if taking orally. Can cause ONH decreased perfusion at night. Can have visual hallucinations.

270
Q

ACE Inhibitors

A

Block angiotenosine I to II converstion.
Decrease aldosterone formation to decrease blood volume and CO. Prevent bradykinin inactivation–>vasodilation. May cause angioedema around the eyes. Can occur at anytime taking the meds.

271
Q

ARBs

A

Stop binding of angiotensin II and blocks aldosterone secretion. Vasodilation and decreases resistance. No effect on bradykinins. Olmesartan medoxomil (approved for pt. from 6-16yo)

272
Q

CCB

A

Decrease Ca in smooth muscle=vasodilation
Decrease heart rate and decrease cardiac output. If pt on oral CCB topical B-blockers can increase risk of AV block, bradycardia, and hypotension. Some studies think CCB protect from glaucoma.

273
Q

Renin inhibitors

A

Inhibits renine from producing angiotenosin I. Can be added to other meds to keep BP study

274
Q

CNS meds

A

Acts centrally to inhibit sympathetic vasomotor centers. Available as a patch

275
Q

Alpha Blockers

A

Relaxes venous and arterial smooth muscle. Not used much as caused CV dz. Can cause intraoperative floppy iris syndrome. Poor pupil dilation and iris prolapse during cataract surgery.

276
Q

JNC8 medications for nonblack pop of any age?

A

Thiazide diuretics, CCB, ACEI, ARB. No beta blockers dur to neg. outcome of one study

277
Q

JNC8 medications for general black pop of any age?

A

Thiazide and CCB. ACEI increase stroke in black pop.

278
Q

JNC8 meds for those with CKD and HTN 18+ years regardless of race or diabetes.

A

ACEI or ARB. Can prescribe with or without proteinuria. No literature supports for 75+

279
Q

Which drugs should not be used in combination?

A

ACEI and ARB!

CCB and topical Beta blockers!

280
Q

HTN and glaucoma

A

Noctural hypotension is a risk for increased POAG and NTG. Must look for the dippers! There are compliance issues in both!

281
Q

Marfan Syndrome

A

CT disorder with abnormalities of skeletal, cardiovascular, and ocular system. Autosomal dominant disease. Difficult to diagnose as var. signs and symptoms.

282
Q

Char. of those with Marfan

A
  1. Skeletal-Narrow face, tall and slender, long legs, arms fingers, loose joints. Scoliosis, chest deformities, diminished reflex, diminished muscle tone. Strech marks without previous weight gain.
  2. Ocular-Will find bilateral ectopic lentos, axial myopia, strabismus (20), iris transillumination (10), retinal detachment, glaucoma (8), cataracts, peripheral retinal degnerations, blue scleras due to thinness. . 3. Cardiovascular dz in almost all. Ascending aortic dilation, aneurysm and dissection. Most common cause of death which can be sudden. Aortic regurgitation. Mitral valve prolapse
  3. Pulmonary system-increased risk of pneumothorax or obstructive sleep apnea.
283
Q

DZ of Marfan

A
  1. Family history-not necessary but makes easy
  2. Ocular exam-finding bilateral ectopic lens
  3. Echocardiography and EKG
  4. CT or MRI imaging to assess aortic size-dilation of aorta
  5. Physical exam
  6. DNA analysis can deltic mutations in the fibrillin gene on chromosome 15.
284
Q

Tx for Marfan

A

There is no cure

  1. Decrease CV complication with beta blockers, acei, CCB, or ARBs
  2. Composite grafts to replace aorta valve and aneurysms
  3. Prophylaxis for bacterial endocarditis. AB given before invasive procedure.
  4. avoid exercise and contact sports
  5. Pain meds
285
Q

Referal with Marfans

A

If they are undiagnosed, have moderate scolosis, to get annual cardiological evaluate, if pregnant or need genetic counseling. Any pt. with severe chest pain would be hospitalized ASAP!

OPT 537 - OWN (2 decks)

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