Starting at 115/75, CVD risk goes up by () with each increment of 20/10
Hypertension causes kidney disease via
Malignant HTN and Chronic Hypertensive Nephrosclerosis.
If your less than 60, BP should be
If your more than 60, BP should be
If CKD, BP should be
Increased cGMP + Reduction in Sympathetic Tone -> Vasodilation, Decrease Renin -> Natiuresis and Diruesis Decreased Blood Volume -> Decrease Blood Volume and Pressure. Arterial, venous and coronary vasodilation.
Glomerulonephritis causes HTN by...
Resistance to ANP. More HTN. Increase in Na/K ATPase.
Flash pulmonary edema
Bilateral RAS and ACE-I.
Signs of RAS
Flash pulmonary edema with ACEi/ARB; Increase in creatinine by >30% on initiation of ACEi or ARB; Asymmetric Kidney sizes; newly difficult to control BP in a patient formerly well controlled.
Renin and aldosterone. U/S, MRA, CT.
Angiotensin II to AT1 receptors leads to blood vessel contraction and
Adrenal cortex aldosterone secretion via increasing desmolase activity (rate limiting step of steroid synthesis) and aldosterone synthase.
Fibromuscular dysplasia association
String of beads
Fibromuscular dysplasia diagnosis
String of beads; increased renin and aldosterone (from turbulent blood flow); u/s, MRA, ct angiogram.
Why string of beads
Alternating aneurysmal dilatation -> hypertrophy constriction/ stenosis -> aneurysmal...Etc. Defect in artery – intima, media or adventitia. Most common in media. Lack internal elastic lamina in the aneurysms.
Which type of Scleroderma may have renal crisis
Diffuse cutaneous systemic sclerosis (Vs CREST). Collagen is all over the place – mask facies, sclerodactyl, etc. And even at arteries around kidney as well making for pinpoint openings.
CREST syndrome, CREST stands for
CREST involvement: Calcinosis, Raynaud phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasia. More benign clinical course.
Sclerodermal renal crisis diagnosis
Increased renin and angiotensin. Renal biopsy too. Abrupt moderate to severe htn with quick and rapid AKI.
Sclerodermal renal crisis treatment
ACEi or ARB.
Liddle’s syndrome is
Overactive ENaC. Limited to kidney itself (transplant kidney and it will go away).
Liddle’s triad of symptoms
Early age HTN, Hypokalemia and Metabolic Alkalosis.
Low renin and aldosterone.
Amiloride (or triamterene).
More CKD, lower GFR, means...
Malignant HTN presentation in eye
Flame hemorrhages; papilledema, cotton wool spots, hard exudates and bulging of disc.
With moderate BP elevation, how does kidney respond
Vasoconstriction. Wants to prevent increase in pressure from being transmitted to smaller more distal vessels. Smaller vessels also have tensile strength. But in severe cases, autoregulation reaches a limit.
Most common is E. Coli but Staph Saprophyticus is common too. (And proteus, klebsiella, enterococcus fecalis).
Nosocomial pathogens causing UTI
Citrobacter, Serratia, Pseudomonas, Candida as well as E. Coli.
Sterile pyuria and negative urine cultures suggest
Neisseria Gonorrhea or Chlamydia.
4 key bugs
E. Coli, Staph saprophyticus, Klebsiella, Proteus.
Risk factors for UTI in young
Female sex, sexual intercourse, indwelling catheter, history of UTI (-> more adhesion receptors on genitourinary mucosa; also may lack fucosyl transferase activity), DM, impaired bladder emptying, parity.
Risk factors for UTI in older
AD, PD, CVA and men – BPH, stricture and women – loss of estrogen, incomplete emptying of bladder, urethroceles, bladder diveritcula.
Why does foreskin have propensity for colonization
Propensity for colonization with P-fimbriated bacteria.
How does prostate protect from UTI?
Zinc in prostatic secretion prevents ascending infections.
Infection in a patient with structurally and functionally normal urinary tract. Most isolated or recurrent cystitis and pyelonephritis and usually short course of antibiotics.
Infection in a patient with structural or functional impairments that would reduce efficacy of anti-microbial therapy.
Not treated unless obstruction or DM or pregnancy.