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Clin Path Final Q7 > Clin Path Final > Flashcards

Clin Path Final Flashcards

1
Q

What can cause strile pyuria?

A

recent UTI with antibiotic treatment, glucocoticoids, acute febrile episodes, pregnancy.

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2
Q

What is pyelonephritis?

A

Kidney infection caused by hematogenous spread or retrograde spread of pathogenic microorganism.

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3
Q

What are the 2 types of pyelonephritis?

A

Acute and chronic.

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4
Q

What is the clinical presentation of acute pyleonephritis like?

A

fever, flank pain, nausea, costovertebral angle tenderness, cystitis symptoms, sepsis/shock.

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5
Q

What will the onset of acute pyleonephritis be like?

A

Acute onset.

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6
Q

What is seen in urine with acute pyelonephritis?

A

Marked pyuria, WBC clumps, WBC casts and proteinuria.

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7
Q

What should you think of when you have WBC clumps and WBC casts?

A

Clumps- bladder infections. Casts- kidney infections.

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8
Q

What is a chronic pyelonephritis like?

A

Fewer findings that acute and not grossly pyuric and may have some clumps and casts.

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9
Q

What is cystitis?

A

An inflammed bladder usually caused by an infected bladder.

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10
Q

Who will be more likely to get a bladder infection?

A

Women.

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11
Q

What are the presentations of cystitis?

A

Dysuria, frequency, urgency, suprapubic pain, fever, nausea, PAINFUL GROSS HEMATURIA.

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12
Q

What are the routine findings on urinalysis for a cystitis?

A

hematuria, pyuria, nitrite, alkaline pH, bacteriuria and proteinuria.

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13
Q

What tests on a urinalysis will show up with bacteriuria?

A

Leukocyte esterase and nitrite.

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14
Q

What is a normal history of a women with cystitis?

A

recent sex, used spermicide, previous history of UTI, Maternal history of UTI.

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15
Q

What will decrease the likelihood of an acute urinary tract infection for females?

A

vaginal irritation and or discharge.

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16
Q

What are the 3 types of prostatitis?

A
  1. Acute bacterial prostatitis. 2. chronic bacterial prostatitis. 3. Nonbacterial prostatitis.
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17
Q

What causes acute bacterial prostatitis?

A

gram negative coliform bacteria that ascends from urethra, refluxes into prostate from infected urine or could spread via lymph from rectum or hematolgenously from another infection.

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18
Q

What are the clinical symptoms of acute bacterial prostatitis?

A

fever, chills, low back and perineal pain, urinary urgency and frequency, nocturia, dysuria, bladder outlet obstruction, myalgias and arthralgias.

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19
Q

How will acute bacterial prostatitis be diagnosed?

A
  1. Prostate palpation (swollen, tender and warm). 2. lab- leukocyte shift to the left, pyuria with mild hematuria, cloudy malodorous urine with gross hematuria. 3. prostatic expressate is purulent and can be cultured.
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20
Q

What is more common acute or chronic bacterial prostatitis?

A

Chronic.

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21
Q

What causes chronic bacterial prostatitis?

A

Etiology is similar to acute and may be due to gram positive bacteria.

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22
Q

What is the history like for chronic bacterial prostatitis?

A

Usually no history of previous acute bacterial prostatitis.

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23
Q

What are the clinical symptoms of chronic bacterial prostatitis?

A

range from asymptomatic to irritative voiding dysfunction (nocturia, dysuria, urgency, frequency), back or perinal pain.

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24
Q

What will prostate palpation and lab findings be like for chronic bacterial prostatitis?

A

palpation ranges from normal to slightly boggy to focal indurations, lab- hazy prostatic expressate due to WBC’s.

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25
Q

What are some possible causes of nonbaceterial prostatitis?

A

Etiology is unkonwn but could be from caffine, alcohol, and spicy foods.

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26
Q

What is more common chronic bacterial or nonbacterial prostatitis?

A

Nonbacterial prostatitis.

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27
Q

What are the findings with nonbacterial prostatitis?

A

Similar to chronic bacterial prostatitis with negative cultures of prostate expressate.

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28
Q

What is urethritis and what are the 2 types?

A

Inflammation of the urethra. Gonococcal and nongonococcal.

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29
Q

Gonococcal urethritis commonly effects who?

A

Males.

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30
Q

What are the clinical sings and symptoms of gonococcal urethritis?

A

penial discharge, dysuria, urethral itching.

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31
Q

What labs should be done with gonococcal urethritis?

A

Not urinalysis since it should be done CCMS. The penile discharge should be collected 1-4 hours after voiding and be cultured.

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32
Q

What is the difference between gonococcal and nongonococcal urethritis?

A

Nongonococcal has same signs and symptoms but is often caused by chlamydia.

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33
Q

What is another name for hypertension that damages the kidneys?

A

nephrosclerosis.

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34
Q

What type of damage is done to the kidneys with hypertension?

A

serious and irreversible renal damage.

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35
Q

What is the age of onset for nephrosclerosis to take place?

A

30-60 years with a history of hypertension for 2-6 years.

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36
Q

Hypertension can cause a type of what?

A

chronic renal failure.

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37
Q

What are the laboratory evidence of renal damage from hypertension?

A

Anemia, mild proteinuria and hematuria (in early stages). Marked proteinuria, hematuria, urinary casts (late stages).

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38
Q

With nephrosclerosis (kidney damage due to hypertension) what would indicate chronic renal failure is taking place?

A

Azotemia.

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39
Q

What is nephrolithiasis?

A

Urinary stone disease or kidney stones.

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40
Q

Nephrolithiasis is the ____ most common urinary tract problem.

A

Third.

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41
Q

What is the first and second most common type of urinary tract problems?

A
  1. infections. 2. prostatic disorders.
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42
Q

What are the main type of kidney stones?

A

Those made of calcium salts.

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43
Q

How much more common are kindey stones in male than females?

A

4:1 in 20’s and 30’s in 50-60’s 1:1.

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44
Q

Incidnec of nephrolithiasis increased with who?

A

Sedentary lifestyle, summer months and humidity.

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45
Q

What factors promote stone formation?

A

Diets- exess sodium, excess protein, high calcium, high oxalate and purines. Dehydration, stress, chronic infections.

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46
Q

What factors will inhibit stone formation?

A

citrate, increased water intake.

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47
Q

What is the most common symptoms with nephrolithiasis?

A

Pain.

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48
Q

What is the pain like for kidney stones?

A

one of the most intense pains suffered by humans, but may be dull and persistant. May refer to testis or labium as stone moves through ureter.

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49
Q

What will the patients response to the pain be?

A

they tend to move about due to pain but cant get relief.

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50
Q

What are the laboratory findings for nephrolithiasis?

A

micro or gross hematuria. Possible increase in WBC if infection if present.

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51
Q

What are the 2 types of urinary tract obstructions?

A

congenital and aquired.

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52
Q

What are the 3 areas of urinary tract obstructions?

A
  1. Ureter. 2. bladder outlet. 3. urethra.
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53
Q

What are the acquired causes of bladder outlet obstructions?

A

bladder cancer, benign prostatic hyperplasia, prostate cancer.

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54
Q

What is the mean age of a diagnosed bladder cancer?

A

65 years.

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55
Q

What is the male:female ratio for bladder cancer?

A

3:1 male-to-female.

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56
Q

What are the known risk factors for bladder cancer?

A

Smoking, industrial dyes and solvent exposure.

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57
Q

What are the clinical findings of bladder cancer?

A

ranges from none to irritative voiding.

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58
Q

What are the lab findings seen with bladder cancer?

A

chronic hematuria gross or micro, pyuria, azotemia, anemia, abnormal urothelium.

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59
Q

What type of imaging should be done for bladder cancer?

A

intravenous urography, ultrasound, CT or MRI, cystourethroscopy.

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60
Q

Who is most likely to get benign prostaitic hyperplasia?

A

50% of men by the 6th decade of life.

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61
Q

What causes benign prostatic hyperplasia?

A

Not totally understood. Has association with endocrinologic (dihydrotestosterone- associated with hair loss).

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62
Q

What are the 2 types of complaints seen with benign prostatic hyperplasia?

A

Obstructive and irritative.

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63
Q

What things are seen with obstructive complaints (benign prostatic hyperplasia)?

A

hesitancy, decreased force and caliber, sensation of incomplete bladder emptying, double voidint (twice within 2 hours), straining and postvoid dribbling.

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64
Q

What things are seen with irritative complaints (benign prostatic hyperplasia)?

A

Urgency, frequency, nocturia.

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65
Q

What lab tests can be done for Benign prostatic hyperplasia?

A

some to rule out DDx like; Urinalysis to rule out infection, serum creatinine to assess renal function, and serum PSA to help rule out prostate cancer.

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66
Q

What type of cancer is the most common cancer detected in American men?

A

Prosate cancer (not benign prostatic hyperplasia).

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67
Q

How common is prostate cancer?

A

40% of those over 50. 70% of those 80-89.

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68
Q

Where is prostate cancer most common at?

A

North America and Europe. Lowest is in Far East.

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69
Q

What are the risk factors for prostate cancer?

A

Family history, blacks, fatty diets.

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70
Q

How are prostatic cancers detected currently?

A

Digital rectal examinations (DRE).

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71
Q

What are the findings seen with DRE for prostatic cancer?

A

Focal nodules, areas of indurations.

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72
Q

Besides DRE what is another way to detect prostatic cancer?

A

prostate specific antigen test. Transrectal ultrasound (TRUS). Biopsy. History- signs of urinary retention and obstructive voiding symptoms are rare and most often due to benign prostatic cancer.

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73
Q

What is the most accurate way to detect prostatic cancer?

A

Biopsy.

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74
Q

How accurate is TRUS?

A

lacks specificity and leads to too many biopsies.

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75
Q

What is PSA?

A

a glycoprotein produced in the cytoplasm of prostate cells.

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76
Q

Why would PSA serum levels be helpful in detecting prostate cancer?

A

They will correlate in volume in serum for benign and malignant prostatic tissues and will be helpful in detecting and staging the disease.

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77
Q

What is a good number for normal PSA levels?

A

Depends on age but less than 2 is good usually (but could still have cancer).

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78
Q

What is a PSA density?

A

A ratio of Serum PSA concentration and prostate volume as determined by TRUS.

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79
Q

What is a better way to monitor serum PSA besides PSA density?

A

PSA velocity- see how much PSA levels increase over a period of time.

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80
Q

What is a good and a bad PSA velocity?

A

greater than 0.75 increases the likelihood of cancer. Those with 0.35 or less have a 92% prostate-cancer-survival rate.

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81
Q

What are the different types of PSA?

A

2 types; 1. Complexed form (complexed with different proteins). 2. Free PSA.

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82
Q

What will the levels of the different types of serum PSA be like with prostatic cancer?

A

Cancer cells produce less free PSA by % even though the total PSA levels increase. >25% free PSA unlikely to have cancer. <10%= 50% chance of cancer.

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83
Q

Total PSA levels below what will have a low risk of prostatic cancer?

A

below 2-2.5.

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84
Q

Total PSA levels above what will have a high risk of prostatic cancer?

A

Abover 10.

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85
Q

What should be done when the lab total PSA levels show somewhere between 2.5-10?

A

See if the % of free PSA is within normal limits(below 10%).

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86
Q

What should be done if DRE and PSA levels indicate prostatic cancer?

A

Biopsy if life expectancy is greater than 10-15 years since prostatic cancer has about 10-15 survival rate.

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87
Q

What should you think of when you hear painless gross hematuria?

A

Kidney tumor until proven otherwise.

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88
Q

How common is renal cell carcinoma? When is the peak incidence?

A

3% of all reported cancers. Peak incidency in 6th decade of life.

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89
Q

Who is more likely to get renal cell carcinoma Male or females?

A

males 2x as common as females.

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90
Q

What is a risk factor for renal cell carcinoma?

A

Cigarette somking.

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91
Q

What are the clinical findings seen with renal cell carcinoma?

A

ranging from none to flank pain, abdominal mass, and symptoms of metatstaic diseases like cough or bone pain.

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92
Q

What are some common signs and symptoms seen with renal cell carcinoma?

A

Hematuria, abdominal pain, palpable mass in the flank or abdomen.

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93
Q

What are some non-specific symtoms and signs of renal cell carcinoma?

A

fever, night sweats, weight loss, malaise.

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94
Q

When will most renal cell carcinomas be detected?

A

As incidental detectino due to increased use of CT and US for diverse reasons.

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95
Q

What are the lab findings seen with renal cell carcinoma?

A

Hematuria (gross or microscopic), anemia (due to loss of EPO), erythrocytosis (due to increased kidney cells that make EPO), hypercalcemia, elevated alkaline phosphatae (with bony metastasis).

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96
Q

What is a shift to the left?

A

Increase in the number of immature neutrophils in peripheral circulation called band cells or band neutrophils which is indicitive of an acute infection.

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97
Q

What is the philidelphia chromosome responsible for?

A

95%- CML. 5%- down syndrome.

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98
Q

What is myelofibrosis (with myeloid metaplasia)?

A

fibrotic replacement of bone marrow in response to increased secretion of platelet derived growth factor and this causes extramedullary hematopiesis and the hematopoisis is less competent.

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99
Q

What are the signs and symptoms of myelofibrosis (with myeloid metaplasia)?

A

abdominal fullness, fatigue (due to anemia).

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100
Q

What are the lab findings with myelofibrosis (with myeloid metaplasia)?

A

anemia with teardrop shaped (dacrocytes) RBC, Variable WBC count, variable platelet count with often bixarre shaped platelets.

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101
Q

What are the signs and symptoms of essential thrombocythemia (ET)?

A

thrombosis is most common problem anc occurs in unusual places like mesenteric, hepatic,and portal veins. Bleeding due to too many platelets that spontaneously aggregate (epistaxis), GI bleeding, hemoptysis and fatigue. Splenomegaly is possible.

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102
Q

What are the lab findings like for ET?

A

Extreme elevation of platelets that are not functional (can be as high as 14,000 reference is 150-450), RBC count can be elevated, IDA (iron deficiency anemia) due to chronic bleeding.

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103
Q

Name 2 types of chronic lymphoproliferative leukemic disorders?

A
  1. Chronic lymphocytic leukemia (CLL). 2. Hairy cell leukemia (HCL).
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104
Q

Who is more likely to get chronic lympocytic leukemias?

A

males 2X greater than females and happens 90% of the time in people over 50.

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105
Q

What are the signs and symptoms of CLL?

A

immunosuppresion, bone marrow failure, lymphocytes inflitate organs, fatigue, reduced tolerance to exercise, hepatosplenomegaly, lymphadenopathy, (in more severe cases; brusing, pallor, fever, infections, weight loss, bone tenderness).

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106
Q

When will CLL be detected usually?

A

Most cases are detected incidentally via a routine CBC as symptoms develop insidiously.

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107
Q

What are the lab findings like for CLL?

A

Lymphoctyosis with mature appearace and are immunoincompentent, anemias and thrombocytopenia are mild early and may get worse.

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108
Q

Who is more likely to get hairy cell leukemias?

A

Males 5:1 with average age of onset at 55 years old.

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109
Q

What are the signs of HCL?

A

gradual onset of fatigue, weakness, abdominal fullness due to splenomegaly, infections, lymphadenopathy.

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110
Q

What are lab findings like for HCL?

A

Pancytopenia, anemia, thrombocytopenia, monocytopenia, and abnormal appearing B cells that look like hairy cells.

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111
Q

What are plasma cell dyscrasias?

A

Malignant disorders of the differentiated end-cells of B-lymphocytes, plasma cells and plasmatoid lymphocytes.

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112
Q

Name the 3 types of plasma cell dyscrasisa?

A
  1. Multiple myeloma. 2. Waldenstrom macroglobulinemia. 3. Monoclonal gammopathy of undetermined significance (idiopathic monoclonal gammopathy).
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113
Q

What are the signs and symptoms of multiple myeloma like?

A

Low back pain is the most common initial symptom.

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114
Q

What is happening with multiple myeloma?

A

a clonal proliferation of malignant plasma cells that begins in the bone marrow and dissemiates to involve multiple bony and visceral sites.

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115
Q

Multiple myeloma is the most common malignat disease of what?

A

Plasma cells.

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116
Q

Who is most likely to get multiple myeloma?

A

People over 50 and is as common as 2-3 per 100,000.

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117
Q

What happens when the malignant prolferation of a single clone of a plasam cell (multiple myeloma) infiltrates the marrow?

A

Thrombocytopenia- bleeding, leukopenia- infections, pancytopenia- anemia (weakness and fatigue).

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118
Q

What happens when the malignant prolferation of a single clone of a plasam cell (multiple myeloma) destroyes skeletal tissue?

A

Osteoclastic activating factor, expanding plasmacytomas, pathological fractures, lytic bone lesions- which leads to hypercalemia, osteopenic changes- bone pain.

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119
Q

How will multiple myeloma change proteins?

A

decreases normal immunoglobulins- infections. Also creates abnormal proteins like bence-jones which leads to kidney failure, and monoclonal gammopathy which leads to hyperglobulinemia and M-spike on SPEP (serum protein electrophoresis).

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120
Q

What are the common clinical findings seen with multiple myeloma?

A

skeletal pain, infections, anemia, kidney dysfunction- due to bence-jone proteins, hyperviscosity syndrome.

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121
Q

What will hypervisocity syndrome lead to?

A

mucosal bleeding, vertigo, nausea, visual distrubances, and altered mental status.

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122
Q

What are the hematolgy lab tests like for multiple myeloma?

A

Normacytic and normochromic anemai, rouleaux formation, WBC and platelet counts are normal if early in the disease, late will show pancytopenia.

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123
Q

What are the serology lab tests like for multiple myeloma?

A

Markedly elevated ESR due to hypergammaglobulinemia.

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124
Q

Will serology labe tests for multiple myeloma that show elevated ESR due to hypergammaglobulinemia be a good way to diagnose Multiple myeloma?

A

No.

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125
Q

What will routine serum protein tests show for multiple myeloma?

A

increased total protein, increased globulin, decreased A/G ratio due to increased globulins and will have normal albumin, hypercalcemia in about 10% of patients, azotemia (increased Blood urea nitrogen(BUN)), increased uric acid as renal failure develops.

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126
Q

Since there are increased amounts of globulins seen with multiple myeloma a serum protein electrophorisis should be done to determine what type of globulins are inceased and what will they be?

A

Gamma globuins - IgG will show the M-spike seen in 80% of multiple myeloma patients.

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127
Q

How is a bence-jones protein detected?

A

Not on a routine urinalysis, but is found on urine electrophoresis or heat precipitation tests.

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128
Q

How common are bence-jones proteins with multiple myeloma?

A

75% of patients with MM will have them.

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129
Q

What are the differences between patients with bence-jones proteins and without?

A

With- light chain myeloma and is a more aggressive malignancy. Without- non-secretory myeloma- very uncommon but is uncommonly aggressive.

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130
Q

What type of protein is bence-jones?

A

M-paraprotein.

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131
Q

What will a routine urinalysis show for multiple myeloma patients?

A

Proteinuria, hematuria, hyaline casts, renal tubular epithelial cells, cellular casts as renal failure develops.

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132
Q

What is the definitive way to diagnose someone with multiple myeloma?

A

Bone marrow aspiration.

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133
Q

What is waldenstrom macroglobulinemia?

A

A malignancy of B-lympocytes with increased levels of IgM.

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134
Q

What are the clinical findings seen with waldenstrom macroglobuinmeias?

A

Fatigue, weight loss, blurred vision, bleeding episodes especially epistaxis, hepatosplenomegaly, lymphadenopathy, retinal abnormaliteis including hemorrhage.

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135
Q

What are the lab results for Waldenstrom macroglobulinemias?

A

normocytic normachromic anemia with rouleaux formation, leukocytes and platelet counts normal, elevated ESR, IgM hypergammaglobulinemia, urine free light chains (B-J proteins) in about 25%, prolonged bleeding time.

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136
Q

What is monoclonal gammopathy of undetermined significance?

A

Monoclonal protein production in the absence of disease seen in the elderly and can possilby be a pre-myeloma condition.

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137
Q

What are lab findings like for monoclonal gammopathy of undtermined significance?

A

Serum proteins similar to multiple myeloma, bone marrow is normal.

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138
Q

What are lymphomas?

A

a group of disorders which primarily manifestation is neoplastic prolferation of lymphocytes leading to abnormal lymph node enlargement which is painless.

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139
Q

How are lymphomas diagnosed?

A

Via lymph node biopsy.

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140
Q

Name the 2 types of lymphomas?

A

Hodgkin disease, and nonhodgkins lymphoma

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141
Q

What is hodgkin’s disease like?

A

Malignant lymph node with reed-sternbery cells.

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142
Q

What are the clinical findings seen with Hodgkins disease?

A

Painless enlarged lymph nodes especially in ceck and might be painful due to rapid growth, fever, night sweats, weight loss.

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143
Q

What are the lab findings for hodgkins disease?

A

early on- eosinophilia. Later- leukocytosis, granulocytosis, lymphocytopenia, N/N anemia.

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144
Q

What is nonhodgkins lymphoma?

A

effects B-lymphocytes 95% of the time and T-lymphocytes 5% of the time.

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145
Q

What are the clinical findings seen with nonhodgkins lymphoma?

A

Painless cervical lymph node enlargment, fever, weight loss, night sweats.

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146
Q

Wha tare the lab findings like for nonhodgkins lymphoma>

A

Blood counts essentially normal until late in disease, positive direct coombs test, leukemic phase.

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147
Q

What is the spread of hodgkins and nonhodgkins lymphoma like?

A

Hodgkins is predictable. Nonhodkins is less predictable involves multiple lymph nodes and nonlymphoid tissues more commonly than HD.

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148
Q

What level of hematuria warrants investigation?

A

Any level should be inspected to see where it came from.

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149
Q

What will make a urinalysis positive for blood (hematuria)?

A

A reagent strip that says there is blood or more than 3 RBC/hpf.

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150
Q

Hematuria may be the only and first sign of what?

A

Early urinary tract pathology.

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151
Q

What are the 2 categories of hematuria?

A

Without casts or without proteinuria, with casts and proteinuria.

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152
Q

What are the types of hematuria without casts or proteinuria?

A

trauma, lower urinary tract infections, hypertension, bleeding disorders, kidney pathology (stones, tumors).

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153
Q

What are the types of hematuria with casts and proteinuria?

A

acute glomerulonephritis, chronic glomerulonephritis, rheumatoid disease.

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154
Q

Proteinuria may be the first and only sign of what?

A

Early urinary tract pathology.

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155
Q

Name 4 reasons for developing proteinuria?

A
  1. Functional proteinuria (minimal amounts). 2. Overload proteinuria (pre-renal). 3. Glomerular proteinuria. 4. Tubular proteinuria.
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156
Q

Name 4 tests used to evaluate kidney function?

A
  1. Clearance test. 2. Creatinine clearance. 3. Serum blood urea nutrogen. 4. Serum creatinine.
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157
Q

What will the clearance test screen for?

A

Mild to moderate diffuse glomerular damage.

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158
Q

What is creatinine?

A

The end product of skeletal muscle metabolism.

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159
Q

What will levels of creatinine in serum represent?

A

skeletal muscle mass not activity.

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160
Q

When will levels of creatinine be increased and decreased?

A

Increased- renal disease and increased muscle mass. Reduced- females and children and people with decreased muscle mass.

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161
Q

The serum creatinine levels have the same significance as what?

A

Renal azotemia.

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162
Q

What is BUN?

A

Blood urea nitrogen that is a non-protein nitrogenous waste from protein metabolism that liberates AA and the AA go to the liver and become urea which goes to the kidneys and is placed in urine.

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163
Q

Increased BUN equals what?

A

Azotemia.

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164
Q

What level of kidney function is needed for the exrection of BUN and creatinine?

A

only 50%.

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165
Q

What are the 7 key elements that would lead one to think of kidney problems?

A
  1. Urine volume changes. 2. Abnoramlities of urine sediment. 3. Abnormal excretion of urine proteins. 4. Reduction in GFR (azotemia). 5. Hypertension and or edema. 6. Electrolyte abnormalites. 7. fever and or pain (flank or suprapubic).
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166
Q

What is acute renal failure?

A

sudden loss of renal function due to extreme medicla etiologies. Leading to a decreased renal perfusion or obstruction of outflow from kidneys.

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167
Q

What is acute nephritis (aka nephritic syndrome or acute glomerulonephritis)?

A

an acute inflammatory process initiated by immune complexes that deposit onto or in the glomeruli, renal vasculature, interstitium and tubular epithelium and causes inflammatory changes.

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168
Q

What happens with damaged glomerular walls with acute nephritis?

A

They allow the escape of RBC’s and proteins into glomerular filtrate which results in cast formation

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169
Q

What happens to urine output levels with acute nephritis?

A

There will be an acute reduction in glomerular filtration rate (GFR) and this results in oligouria.

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170
Q

Oligouria can result in what?

A

Salt and water retention which can lead to hypertension, edema, headache, blurred vision.

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171
Q

What type of infections can lead to acute nephritis aka glomerulonephritis?

A

Lancefield group A beta-hemolytic streptococcus (Strep throat).

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172
Q

What happens after someone gets strep throat?

A

There can be a latent period of 6-10 days between infection and nephritis.

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173
Q

How can a postinfectious or poststreptococcal glomerulonephritis be diagnosed?

A

Clinical history with signs and symptoms Plus A test= antistreptolysin O which is a test identifying the antibody to streptococcal exonenzymes.

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174
Q

What are some general lab findings seen with an acute nephritis?

A

Hematuria, RBC casts, proteinuria, azotemia.

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175
Q

What is Chronic renal failure (CRF)?

A

Progressive and irreversible destruction of nephrons regardless of the cause.

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176
Q

What is required for a CRF diagnosis?

A

3-6 months of documented redution in GFR, Anemia, Hypocalcemia (hyperphosphatemia), urinary protein and broad casts.

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177
Q

Why will CRF patients be anemic?

A

Kidney cant make enough EPO.

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178
Q

Why will CRF patients have hypocalcemia and hyperphosphatemia?

A

With kidney damage there is less vitamin D3 turned into its active form and there will be less calcium when there is less calcium there will be more phosphate.

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179
Q

What are the 3 stages of CRF?

A
  1. Diminished renal reserve- measurable loss of renal function. 2. renal insufficiency- azotemia. 3. Uremia.
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180
Q

What is uremia?

A

Fluid or electrolyte balance disturbances, increasing azotemia, systemic manifetation from toxic effects of protein metabolites.

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181
Q

What are the toxic effects seen from protein metabolites?

A

Endocrine-metabolic, neuromuscluar, cardiovascular and pulmonary, dermatologic, GI, hematologic and immunologic.

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182
Q

Broadcasts are usually only seen with what condition?

A

Chronic kidney failure.

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183
Q

Increased specific gravity means what?

A

lost the concentrating ability of the kidney.

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184
Q

What should you think of when you hear nephrotic syndrome?

A

Proteinuria.

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185
Q

What is nephrotic syndrome?

A

This occurs as a consequence of a disease which causes specific types of damage to the glomerular structures.

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186
Q

Name some diseases that cause damage to the glomerular structures?

A

DM, Systemic diseases like lupus, nephrotoxic medications, toxemia of pregnancy.

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187
Q

Nephrotic syndrome is aka?

A

secondary nephrotic syndrom since it is caused by systemic diseases.

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188
Q

What type of things are seen with nephrotic syndrome?

A

Massive proteinuria, generalized emdema, hypoalbuminemia, hyperlipidemia, hyperlipiduria.

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189
Q

What is idiopathic nephrotic syndrome?

A

A type of nephrotic syndrome with an unknown cause.

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190
Q

When will an idiopathic nephrotic syndrome be diagnosed?

A

At childhood.

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191
Q

How is an idiopathic nephrotic syndrome diagnosed?

A

via exclusion of secondary causes and most often requires a renal biopsy.

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192
Q

What would renal function tests be like fro idiopathic nephrotic syndromes?

A

Normal.

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193
Q

What is the prognosis for idiopathic nephrotic syndrome?

A

most types are managed just fine with prednisone and rarely will they progress to end stage renal failure.

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194
Q

Name the different types of urinary tract infections?

A
  1. Sterile pyuria. 2. pyelonephritis. 3. acute pyelonphritis. 4. Chronic low-grade pyelonephritis. 5. urinary bladder infections. 6. prostatitis. 7. urethritis.
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195
Q

What is sterile pyuria?

A

WBC in urine with negative bacteriologic evaluation.

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196
Q

Vasoconstriction

A

platelet granules release serotonin (which causes the vasoconstriction)

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197
Q

Platelet plug formation

A

aggregated platelets release von Willebrand factor which helps allow platelets to stick together. Thromboxane (released from the platelets) promotes aggregation, degranulation, and vasoconstriction.

198
Q

Coagulation

A

split into an intrinsic or extrinsic pathway

199
Q

Intrinsic pathway

A

contact factors changing XI into XIa and results in a series of cascading events that eventually joins the extrinsic pathway and results in a fibrin clot.

200
Q

extrinsic pathway

A

release of factor VII from injured vessels, and causes a series of events that eventually combines with the intrinsic pathway to form a fibrin clot.

201
Q

Primary hemostasis

A

characterized by vasoconstriction, platelet adhesion, and formation of a soft aggregate plug. This occurs about 20 seconds after injury

202
Q

Secondary hemostasis

A

responsible for stabilizing the soft plug. Vasoconstriction is maintained, soft plug becomes solidified , and coagulation factors are produced in liver and circulate until coagulation cascade is initiated

203
Q

Vasoconstriction

A

no routine tests for vasoconstriction

204
Q

Platelet count

A

measures total number of platelets in blood, determined by a routine CBC

205
Q

Bleeding Time (BT)

A

platelet function test, evaluates interaction of platelets with vessel wall and the formation of a plug; test is independent of coagulation.

206
Q

Platelet count test

A

must be done first to ensure that platelets are present before testing the function of platelets

207
Q

Normal postabsorptive levels of glucose

A

Maintained between 60-100mg/dL despite ingestion of food

208
Q

True hypoglycemia

A

1.)Low serum glucose concentration during time patient experiences spontaneously developed symptoms 2.)Whipple’s Triad

209
Q

Whipple’s Triad

A
  1. ) Presence of adrenergic and/or neuroglycopenic signs and symptoms
  2. ) Low plasma glucose measured at time of symptoms
  3. ) Relief of symptoms when glucose is raised back to normal (relieved by administration of glucose)
210
Q
  1. Adrenergic signs and symptoms of hypoglycemia
A

Hunger, tachycardia, sweating, tremors, fatigue, and anxiety

211
Q

Neuroglycopenic signs and symptoms of hypoglycemia

A

Dizziness, headache, confusion, lethargy, visual disturbances, blunted mental acuity, abnormal behavior, convulsions, and coma

212
Q
  1. postprandial hypoglycemia follows…
A

surgical procedures such as gastrectomy, gastrojejunostomy, pyloroplasty, and vagotomy

213
Q

postprandial hypoglycemia results from…

A

rapid gastric emptying, rapid absorption of glucose, and excessive release of insulin

214
Q

Causes of fasting hypoglycemia: Hyperinsulinism

A

Hyperinsulinism=
Excess insulin administered in diabetic patient
Islet cell hyperplasia/tumor

215
Q

Causes of fasting hypoglycemia: DRUGS

A

Alcohol, salicylates in children, and fluoxetine

216
Q

Causes of fasting hypoglycemia: Acquired liver disease

A

Severe hepatitis or cirrhosis

217
Q

Causes of fasting hypoglycemia: hormone deficiencies

A

Hypopituitarism

Adrenal insufficiency

218
Q

Causes of fasting hypoglycemia: Extrapancreatic tumors

A

Carcinoma of liver
Gastrointestinal tract
Adrenal gland

219
Q

Causes of fasting hypoglycemia: Substrate deficiency

A

Malnutrition or late pregnancy

220
Q

Causes of fasting hypoglycemia: Enzyme defects

A

G-6-P or pyruvate carboxylase

221
Q

Idiopathic postprandial syndrome

A

a collection of clinical signs and symptoms similar to medical hypoglycemia but w/o the demonstrably low blood glucose levels.

222
Q

Idiopathic postprandial syndrome signs/ symptoms?

A

Episodes typically occur a few hours after a meal; altered mood and cognitive efficiency, often accompanied by weakness and adrenergic symptoms such as shakiness.

223
Q

Common chronic MACROvascular complications of diabetes

A

Atherosclerosis

224
Q

Common chronic microvascular complications of diabetes

A

Nephropathy, neuropathy, and retinopathy

225
Q

Common cause of T1 DM (Type 1 DM)

A

Immune mediated diabetes= cellular mediated autoimmune destruction of Beta-cells- leads to absolute insulin deficiency.
Circulating insulin is absent, plasma glucagon is elevated, and pancreatic Beta-cells fail to respond to all insulinogenic stimuli

226
Q

Uncommon cause of T1 DM

A

Idiopathic

227
Q

Average age of onset of T1 DM

A

Children and young adults w/ peak incidence before school age and again at puberty

228
Q

Common signs and symptoms of T1 DM with Urination, Vision, Weight…

A
  • Increased urination and thirst d/t osmotic diuresis secondary to sustained hyperglycemia
  • Blurred vision
  • Weight loss d/t depletion of water, glycogen, and triglycerides and later one depletion of muscle mass occurs as amino acids are converted to form glucose and ketone bodies
229
Q

Common signs and symptoms of T1 DM Sensory, PH…

A
  • Paresthesia d/t temporary dysfunction of peripheral sensory nerves (clears w/ restored glycemic levels)
  • Ketoacidosis exacerbates dehydration and hyperosmolarity producing anorexia and nausea w/ vomiting (Ketonemia and ketonuria)
230
Q

Common signs and symptoms of T1 DM plasma glucose levels, autoimmunity…

A
  • Plasma glucose >126mg/dL after overnight fast

- Islet autoantibodies frequently present

231
Q

General cause of T2 DM including factors influencing genesis

A

-Insulin resistance w/ relative insulin deficiency.

232
Q

Cause of T2 DM including factors influencing genesis (Beta Cells)

A

-Enough insulin is present to prevent ketoacidosis, but is in adequate at preventing hyperglycemia d/t tissue insensitivity (Beta cells burn out over time)

233
Q

Cause of T2 DM including factors influencing genesis (Diet)

A

Obesity is most important environmental factor
Overtime Beta-cells undergo hyperplasia and secrete more insulin, cells in body become resistant to regular high levels of insulin

234
Q

Criteria for testing for diabetes (T1 or T2) risk factors…

A
  • BMI > 25, Physical inactivity
  • First degree relative with diabetes, High risk race/ethnicity
  • A1C > 5.7% or IFG on previous test
  • Other clinical conditions associated with insulin resistance
  • History of CVD, Hypertension (>140/90mmHg) or under care, HDL cholesterol 250mg/dL
235
Q

Criteria for testing for diabetes (T1 or T2) for women..

A
  • Women who delivered babies >9lbs or diagnosed with GDM

- Women w/ polycystic ovarian syndrome

236
Q

General criteria for testing for diabetes (T1 or T2)

A
  • All adults who are overweight (BMI > 25) with risk factors

- In absence of above criteria, testing should begin at age 45 and be repeated at least at 3-year intervals

237
Q

Criteria for diagnosing diabetes including the critical values T2…

A

1.) A1C >6.5%= (Type II expensive test)
2.) Fasting plasma glucose >126mg/dL
(Type II- No caloric intake for at least 8 hrs)
3.) 2-hour plasma glucose >200 mg/dL

238
Q

Criteria for diagnosing diabetes including the critical values T1…

A

1.) 2-hour plasma glucose >200 mg/dL
2.) Random plasma glucose > 200mg/dL
(Type I-Patient has classic S/S of hyperglycemia)

239
Q

Role of HbA1c in diabetes diagnosis and management

A

HbA1c= blood test that diagnosis/ monitors diabetes. Avg blood glucose measurement over the past 6-12 weeks used in conjunction with home glucose monitoring to make Tx adjustments

240
Q

Gestational Diabetes Mellitus (GDM)

A
  • risk of spontaneous abortion or congenital malformations early in pregnancy
  • Late in pregnancy poor control can result in polyhydramnios, preterm labor, still birth, and fetal macrosomia
  • At high risk for preeclampsia
241
Q

Postpartum clinical courses of a GDM patient

A

If pregnant women has an underlying weakness of controlling blood glucose levels, 10% chance of developing type II diabetes

242
Q

Who, when, and how patients tested for GDM?

A

Pregnant women not known to have diabetes should be screened for GDM at 24-28 weeks of gestation using a 75g 2 hour OGTT.

243
Q

Diagnosis of GDM…

A

GDM Dependedent on palsma glucose values:
Fasting >92mg/dL
1 hr >180mg/dL
2 hr > 153mg/dL

244
Q

Postpartum testing for GDM patient

A

Women w/ Hx of GDM= lifelong screening for development of diabetes at least every 3 years

245
Q

Two prediabetic states…

A
  1. ) Impaired fasting glucose (IFG)

2. ) Impaired glucose tolerance (IGT)

246
Q

Impaired fasting glucose (prediabetic state)

A

(IFG)….

-Non-diabetic patients w/ fasting plasma glucose (FPG) 100-125mg/dL

247
Q

Impaired glucose tolerance (prediabetic state)

A

(IGT)…

Non-diabetic patients with 2hr plasma glucose (2hPG) 140-199mg/dL

248
Q

Risks of Impaired glucose tolerance and Impaired fasting glucose

A

Higher risk for developing diabetes at rate of 1-5% per year

249
Q

IFG diagnosis?

A

Impaired fasting glucose (IFG) is diagnosed with FPG (no caloric intake for 8 hours)

250
Q

Impaired glucose tolerance (IGT) diagnosis?

A
  • IGT is diagnosed with 2hr plasma glucose

- Patient drinks water w/ 76g anhydrous glucose dissolve in it, blood glucose tested 2 hrs after ingestion

251
Q

What dietary element is necessary for the synthesis of thyroid hormones?

A

Iodine

252
Q

Name two thyroid hormones?

A 
T3 = triiodothyronine
T4 = tetraiodothyronine or thyroxine
253
Q

Explain the basic negative feedback loops involved in the control of thyroid function. (ie. explain the HPT axis [hypothalamic-pituitary-thyroid])

A
  1. ) Hypothalamus secretes TRH (thyroid releasing hormone) which stimulates the pituitary to release TSH (thyroid stimulating hormone)
  2. ) TSH acts on thyroid to produce T3 and T4 (T4 secreted > T3)
  3. ) Tissues can convert T4 into the more physiologically active T3
  4. ) High levels of T4 and T3 inhibit the release of TRH or TSH, thus creating a negative feedback loop
254
Q

Hypothalamus secretes?

A

TRH (thyroid releasing hormone) which stimulates the pituitary to release TSH (thyroid stimulating hormone)

255
Q

TSH acts on thyroid to produce ___?

A

thyroid to produce T3 and T4 (T4 secreted > T3)

256
Q

Tissues can convert T4 into __?

A

more physiologically active T3

257
Q

High levels of T4 and T3 inhibit the release of ___?

A

TRH or TSH, thus creating a negative feedback loop

258
Q

Which thyroid hormone is produced in greatest quantities?

A

More T4 is secreted than T3

259
Q

Form of thyroid hormone possessing the greatest physiologic action?

A

T3 is more physiological active than T4

260
Q

Most of the thyroid hormones produced are bound to ___ and [do not] possess physiologic activity.

A
  • Protein bound portion is not physiologically active

- Remaining non-protein bound portion (<1%) possesses physiological activity

261
Q

What Assay that measures both the protein bound and physiologically active portions of thyroxine?

A

Total Serum thyroxine(TT4) – quantifies TOTAL amount of circulating thyroxine

262
Q

Total Serum thyroxine(TT4) measures ___?

A
  • TT4 measures total circulating levels of T4 and TT4 is profoundly affected by altered levels of carrier proteins
  • Over 99% of T4 is bound to TBG and is not physiologically active (Monitoring non-physiological active hormone)
263
Q

Can a patient be euthyroid with an altered TT4 assay?

A

Yes- Certain non-thyroidal illnesses, physiologic, or pharmacologic challenges result in altered TBG production hence altered TT4 assay, yet patient is euthyroid

264
Q

Free thyroxine (FT4) – assay of non-protein bound physiologically active portion of T4

A

Not affected by many non-thyroidal influences

Better indicator of thyroid function

265
Q

What is Free Thyroxine (FT4)?

A

An assay of non-protein bound physiologically active portion of T4 (Better indicator of thyroid function)

266
Q

Effect of an increase in estrogen has upon the TT4 assay result?

A

Increase T4 levels

267
Q

Clinical advantage of the FT41 assay over the TT4 assay?

A

Takes into account the altered levels of TBG production and therefore better reflects the functional status of the thyroid gland

268
Q

Assay that reflects the functional status of the thyroid gland?

A

FT41 assay

269
Q

Two tests are used in calculating the FT41 ?

A

TT4 and the T3U (hence used to called the T7)

270
Q

Difference between the FT 41 and FT 4 assays?

A
  • FT4 is a direct assay of non-protein bound physiologically active T4
  • FT4I is a calculation reflecting levels of circulating free T4
271
Q

FT4I is a calculation reflecting levels of ____?

A

Free T4

272
Q

Advantage to using FT 4 over the FT 41?

A

$

273
Q

FT4 is a direct assay of _____?

A

non-protein bound physiologically active T4

274
Q

How TSH level reflects thyroid function?

A
  • Secreted by anterior pituitary in response to altered T3, T4, or TRH
  • Fluctuations in TSH are most often proportional to circulating levels of T4 and T3
  • Can be used as a single serum test to screen for status of thyroid
275
Q

____ is secreted by anterior pituitary in response to altered T3, T4, or TRH

A

TSH

276
Q

_____ can be used as a single serum test to screen for status of thyroid

A

TSH

277
Q

The single best serologic test for screening thyroid function?

A

TSH

278
Q

Difference between a TT3 and T3RU?

A
  • T3RU…Indirect estimate of T4 when there is normal amounts of thyroid binding proteins
  • TT3…Useful in evaluating hyperthyroidism (TT3 elevated d/t T4 and T3 elevations)
279
Q

T3RU is estimating levels of T4 by estimating the number of ___?

A

unbound thyroid hormone binding sites on serum protein (TBG)

280
Q

TT3 (measures total amount of circulating T3)

A
  • Levels affected by alterations in protein levels

- Useful in evaluating hyperthyroidism (TT3 elevated d/t T4 and T3 elevations)

281
Q

Difference between a TT3 and T3RU?

A
  • T3RU is estimating levels of T4

- TT3 measure total amount of circulating T3

282
Q

Classic signs and symptoms associated with hypothyroidism (constitutional, CV, Pulmonary)?

A

Constitutional=Weight gain, Fatigue, lethargy, and cold intolerance
Cardiovascular= Bradycardia, Soft tissue swelling
Pulmonary= Dyspnea on exertion and sleep apnea
Snoring

283
Q

Classic signs and symptoms associated with hypothyroidism (Gastro, Genito, Musculo)?

A

1.) Gastrointestinal= Ileus (bowel obstruction), Constipation
2.) Genitourinary= Galactorrhea in women, Menorrhagia
3.) Musculoskeletal= Weakness and carpal tunnel syndrome
Muscle cramps, joint pain, and muscle pain

284
Q

Classic signs and symptoms associated with hypothyroidism (Pysch, Derm, Oto)?

A

1.) Neuropsychiatric=Hyporeflexia, ataxia, and dementia
Depression, headache, and paresthesias
2.) Dermatological= Swelling, pallor, or yellow hue, Dry skin
3.) Otolaryngologic= Middle ear effusion, Hoarseness and decreased hearing

285
Q

Hematologic Laboratory changes w/ hyperthyroidism

A

Anemia and hyponatremia
RBC count, Hgb, Hct all decreased
MCV increased

286
Q

Cholesterol Laboratory changes w/ hyperthyroidism

A

Increase in LDL, total cholesterol, and triglyceride

287
Q

Routine chemistry Laboratory changes w/ hyperthyroidism

A

Liver enzymes and CK are both increased

Serum glucose and sodium are low

288
Q

serologic tests used in diagnosing Hashimoto thyroiditis

A

Measure antithyroglobulin antibody (70%) and antithyroperoxidase antibody (95%)

289
Q

thyroprivic hypothyroidism aka…

A

AKA Primary hypothyroidism

290
Q

Causes of thyroprivic hypothyroidism

A
  • Loss of functional thyroid tissue

- Or functional defects in thyroid hormone biosynthesis and release

291
Q

Causes of functional loss of thyroid tissue

A

d/t chronic autoimmune thyroiditis, reversible autoimmune hypothyroidism, surgery or irradiation, infiltrative and infectious disease, or thyroid dysgenesis

292
Q

Causes of functional defects in thyroid hormone biosynthesis and release…

A

d/t congenital defects in biosynthesis, iodine deficiency or excess, or drugs

293
Q

Causes of goitrous hypothyroidism

A

Iodine deficiency decreases thyroid homogenesis. In response TSH is released which causes the thyroid to enlarge and trap iodine; thus, goiter results.
If iodine deficiency is severe, the patient becomes hypothyroid

294
Q

Clinical problems with neonatal hypothyroidism

A

Cretinism could develop
Results in possible feeding problems, lethargy, prolonged postnatal jaundice, delayed stooling and constipation, enlarged protruding tongue, protruding abdomen, cold mottled skin, and sluggish reflexes.

295
Q

TSH levels associated with primary hypothyroidism are ___?

A

increased

296
Q

TSH levels associated with secondary hypothyroidism

A

decreased…Secondary hypothyroidism is d/t pituitary gland not producing enough TSH

297
Q

Alternative term for hyperthyroidism

A

Thyrotoxicosis

298
Q

Classic signs and symptoms associated with hyperthyroidism (constitutional, CV, Pulmonary)?

A 
Constitutional= Weight loss, Nervousness, restlessness, heat intolerance, and fatigue
Cardiovascular= Tachycardia,Palpitations and chest pain
Pulmonary= Dyspnea on exertion
299
Q

Classic signs and symptoms associated with hyperthyroidism (Gastro, Genito, Musculo)?

A 
Gastrointestinal= Borborygmi, Hyperdefecation (diarrhea) and abdominal pain
Genitourinary= Gynecomastia, Amenorrhea, increased urination, decreased libido, and impotence
Musculoskeletal= Osteopenia, Proximal muscle weakness and muscle cramps
300
Q

Classic signs and symptoms associated with hyperthyroidism (pysch, derm, ophthalmologic)?

A 
Neuropsychiatric= Delirium and psychosis
Tremor, anxiety, and depression
Dermatological= Velvety moist skin, acne
Increased sweating and pruritus
Ophthalmologic= Exophthalmos, Sense of irritation, sensitivity to light, double vision, and sense of pressure in eye
301
Q

Ingested substances that can cause hyperthyroidism

A

Iodine
Estrogens (oral)
Heparin
Heroin

302
Q

Cause of T3 thyrotoxicosis

A
  1. ) Autoimmune – Graves’ disease
  2. ) Subacute (de Quervain) thyroiditis (viral infection)
  3. ) Toxic nodules
  4. ) Drug induced (thyrotoxicosis factitia)
303
Q

Grave’s Disease

A

Antibodies attack thyroid and cause it to overproduce thyroid hormones (T3 thyrotocixosis)

304
Q

Drug induced (thyrotoxicosis factitia)=

A

Ingestion of excessive amounts of exogenous thyroid hormone

305
Q

T3 thyrotoxicosis

Requires use of ______ testing

A

anti-thyroid antibody testing

306
Q

Laboratory changes associated with hyperthyroidism

A
  1. ) Hematologic= Hemoglobin usually normal, possible anemia
  2. ) Cholesterol= Total and LDL cholesterol is decreased
  3. ) Routine chemistry= Calcium and alkaline phosphatase is increased
307
Q

Absolute indications for clinically euthyroid patients to be screened for thyroid function

A

Newborns, goiter, history of head/neck radiation, past or present treatment w/ thyroid medications, graves eye disease, and atrial fibrillation or flutter

308
Q

Relative indications for clinically euthyroid patients to be screened for thyroid function

A

History of nonthyroidal autoimmune disease
Unexplained major weight loss or gain
Females over age 50

309
Q

_____ is common, with both bone matrix and mineral decreased

A

Osteoporosis

310
Q

______is unusual, with the bone matrix intact, and mineral decreased.

A

Osteomalacia

311
Q

Describe the changes in both cortical and trabecular bone in osteoporosis.

A

Loss in cortical thickness and loss in number and size of trabeculae of cancellous bone

312
Q
  1. In osteoporosis, the rate of bone formation is _____, and the rate of bone resorption is usually ______.
A

normal bone formation & increased resorption

313
Q
  1. What are the most common sites of pathologic fractures with postmenopausal osteoporosis?
A

Postmenopausal = collapse of spine (dowager’s hump), and fracture of the hip, wrist, and forearms

314
Q

What are the most common sites of pathologic fractures with senile osteoporosis?

A

Senile = fractures in top of femur (femoral neck) or hip fractures

315
Q

Postmenopausal Seconday osteroporosis (Type 1, high turnover osteoporosis)

A

Affects trabeculae after menopause, estrogen levels decrease (estrogen responsible for regulating bone growth and absorption)

316
Q

____ Affects trabecular and is hormonal in origin

A

Postmenopausal (Type 1, high turnover osteoporosis)

317
Q

Senile osteoporosis

A

(Type 2, age related, or low turnover osteoporosis)

318
Q

Postmenopausal osteroporosis

A

(Type 1, high turnover osteoporosis)

319
Q

Senile Osteoporosis (Type 2, age related, or low turnover osteoporosis)

A
  • Natural aging process (normal seen in people over 70 years old)
  • Affects BOTH trabecular and cortical bone
320
Q

Secondary Osteoporosis

A

Caused by use of drug or as a complication to another condition

321
Q

What are the common normal serum chemistry findings associated with postmenopausal osteoporosis?

A

Serum calcium, phosphate, and PTH are normal, Alkaline phosphatase is usually normal but may be slightly elevated

322
Q

What are the common abnormal serum chemistry findings associated with postmenopausal osteoporosis?

A
  • Intact PTH is metabolically active, most commonly assayed
  • Vit. D is converted to 25-OH In liver and then converted to 1,25-(OH)2. in kidney
  • Vit D Conversion is under direction influence of PTH
323
Q

Vitamin D deficiency is very common as a comorbid condition of ________

A

postmenopausal osteoporosis

324
Q

Vit D Conversion is under direction influence of ____

A

PTH

325
Q

List three ways one can be calcium deficient which may lead to osteomalacia?

A

1.) Vitamin D deficiency

  1. ) Defect in metabolism to the active form
    - Vitamin-D dependent rickets type I
  2. ) End organ resistance to vitamin D
    - Vitamin-D dependent rickets type II
326
Q

Vitamin D deficiency

A
  • Significant problem in post-menopausal women and institutionalized elderly
  • Causes are dietary lack, lack of sunshine, and variety of GI problems
327
Q

Defect in metabolism to the active form

Vitamin-D aka…

A

Vitamin D dependent rickets type I: rare, inherited defect in renal synthesis of 1-25 (OH)2D3

328
Q

End organ resistance to vitamin D aka…

A

Vitamin-D dependent rickets type II (1-25 (OH)2D3 resistant rickets): inherited receptor site defect

329
Q

classic clinical findings associated with osteomalacia?

A
  • Bone pain and tenderness
  • Painful proximal muscle weakness (especially in pelvic girdle)
  • Fractures
330
Q

What would assays reveal in osteomalacia?

A 
Calcium: decreased
Phosphorus: decreased
Alkaline phosphatase: increased (may be variable)
PTH: increased
Vitamin D: decreased
331
Q

What is Paget’s disease?

A

Chronic disorder of unknown etiology that displays abnormally softened and enlarged bony material

332
Q

______ Results in highly vascularized, weakened, deformed, and heavily calcified bone with coarsely thickened lamellae and course trabeculae

A

Paget’s Dz

333
Q

What are Paget’s Dz S/S?

A
  • Patients are often asymptomatic
  • Insidious onset of symptoms which may include bone pain, headaches, decreased hearing, increased skull size, spinal stenosis, compression neuropathies, bowing of long bones, and predisposition to osteoarthritis
334
Q

What is Paget’s cause?

A

Unknown

335
Q

Paget’s AKA

A

Osteitis Deformans

336
Q

classic laboratory changes seen in Paget’s disease?

A
  1. ) Marked increase of alkaline phosphatase
  2. ) Increased urinary hydroyproline
  3. ) Difficult to do d/t needing 24hr urine collection w/ a restriction in the diet
  4. ) Increased serum C-telopeptide (CTx)
  5. ) Both of these are products of collagen breakdown due to bone absorption
337
Q

How is Paget’s treated and know the role of CTx?

A
  • Biphosphonates or nasal calcitonin-salamon

- Role of CTx= Used to measure the rate of bone turnover

338
Q

Biphosphonates or nasal calcitonin-salamon are used to treat ______ bone pathology

A

Paget’s

339
Q

CTx is used to?

A

measure the rate of bone turnover in Paget’s

340
Q
  1. What is the most common cause of Primary Hyperparathyroidism (PHPT)?
A

Over secretion of PTH from single parathyroid gland adenoma > multiple gland hyperplasia > or carcinoma

341
Q
  1. What is responsible for causing clinical problems in PHPT?
A

Hypercalcemia

342
Q
  1. Which five systems are often adversely affected in PHPT?
A 
Gastrointestinal 
CNS
Neuromuscular
Bone
Renal
343
Q

adverse affects of Primary Hyperparathyroidism PHPT on kidney?

A

Renal
Nephrolithiasis – kidney stones
Nephrocalcinosis – deposition of calcium salts in the renal parenchyma

344
Q

adverse affects of Primary Hyperparathyroidism PHPT on bone?

A 
Bone
Osteitis fibrosa cystica
Reduction in number of trabeculae
Resorption of phalangeal tufts 
Subperiosteal resorption of digits
Salt and pepper punched out lesions of the skull
345
Q

adverse affects of Primary Hyperparathyroidism PHPT on CNS?

A

CNS

Ranges from mild personality disturbances to severe psychiatric disorders

346
Q

adverse affects of Primary Hyperparathyroidism PHPT on Neuromuscular?

A 
Neuromuscular
Proximal muscle weakness
Easily fatigable
Muscle atrophy
Altered EMG
347
Q

adverse affects of Primary Hyperparathyroidism PHPT on gastro?

A 
Gastrointestinal 
GERD
Vague abdominal complaints
Ulcers
Pancreatitis
348
Q

What would be the classic chemistry changes observed in PHPT?

A

Calcium: increased
Phosphorus: serum is decreased but urinary phosphate is increased
Alkaline phosphatase: increased
PTH: increased (order last if all above are positive)
Urinary hydroxyproline:

349
Q

In ______, Phosphorus serum is decreased but urinary phosphate is increased

A

PHPT Primary Hyperparathyroidism

350
Q
  1. What is the primary cause of Secondary Hyperparathyroidism (HPT)?
A
  • Increased PTH production resulting from hypocalcemia secondary to renal disease and partial resistance of metabolic action of PTH
  • Resulting hyperplasic of parathyroid gland results in increased PTH but fails to produce hypercalcemia
351
Q
  1. What is another name for secondary HPT? [Hint: radiologists like to use this term.]
A

Renal osteodystrophy

352
Q
  1. What would be the classic laboratory findings associated with secondary HPT?
A 
Hypocalcemia
Hyperphosphatemia
Increased alkaline phosphatase
Increased PTH
Altered renal function = azotemia (BUN and creatinine)
353
Q
  1. What is the most common cause of acquired (and usually transient) hypoparathyroidism?
A

Via loss of functional parathyroid tissue

Usually follows neck surgery or radiation therapy to thyroid

354
Q
  1. What are the signs and symptoms associated with hypoparathyroidism?
A 
Tetany
Carpopedal spasm
Tingling of lips and hands
Muscle and abdominal cramps
Psychological changes
355
Q
  1. What are the classic laboratory findings associated with hypoparathyroidism?
A

Hypocalcemia
Hyperphosphatemia
Decreased PTH

356
Q
  1. List 14 types of systemic manifestations that suggest the presence of a rheumatic disease… :(
A
  • Fever of unexplained origin
  • Noninfectious pleuritis, pericarditis, or peritonitis
  • Skin lesions (erythema, nodules, purpura, or membrane ulcerations)
  • Raynaud phenomenon
  • Valvulitis or myocarditis
  • Pneumonitis or pulmonary infiltration
  • Glomerulonephritis or nephrotic syndrome
  • Peripheral neuropathy
  • Central nervous system manifestations
  • Ocular involvement (keratitis, uveitis, conjunctivitis)
  • Lymphadenopathy or splenomegaly
357
Q
  1. Be able to list the three main components of diagnosing a rheumatic disease…
A

clinical, laboratory, imaging

358
Q

clinical components of diagnosing a rheumatic disease…

A 
Host factors – gender/age/ethnicity
Muscolskeletal features
Mode of onset of pain (sudden vs. insidious or traumatic vs. nontraumatic)
Pattern of muscle and joint involvement 
Systemic manifestations
359
Q

laboratory components of diagnosing a rheumatic disease…

A 
Hematology
Normochromic and normocytic anemias commonly found
Chemistry (not useful), 
Serologic profile
Synovial fluid analysis 
Tissue biopsy
360
Q

imaging components of diagnosing a rheumatic disease…

A

Plan film or advance imaging

361
Q

general hematologic changes observed in a rheumatic disease…

A

Anemia, disorders of leukocytes, platelets, and the coagulation system, and hematologic malignancies

362
Q

Antinuclear antibody (ANA) & Creatinine (commonly used to diagnose and monitor kidney disease in patients who have a rheumatic condition) diagnoses..

A

routine serum chemistries that may aid in the diagnosis and management of a rheumatic disease

363
Q

CCP (or anti-CCP) (a protein that can be detected in up to 70% of people in the early stages of rheumatoid arthritis) and diagnoses…

A

routine serum chemistries that may aid in the diagnosis and management of a rheumatic disease

364
Q

C-reactive protein (nonspecific test is used to detect generalized inflammation) and ESR (used to detect inflammation in the body) diagnoses…

A

routine serum chemistries that may aid in the diagnosis and management of a rheumatic disease

365
Q

Complement serum chemisty & CBC (number of white blood cells, red blood cells, and platelets present in a sample of blood) diagnoses…

A

routine serum chemistries that may aid in the diagnosis and management of a rheumatic disease

366
Q

Hematocrit (test for hemoglobin concentration and the number of red blood cells present in a sample of blood) &
RF diagnoses

A

routine serum chemistries that may aid in the diagnosis and management of a rheumatic disease

367
Q

Name the routine serum chemistries that may aid in the diagnosis and management of a rheumatic disease

A

Antinuclear antibody (ANA)
CCP (or anti-CCP) (a protein that can be detected in up to 70% of people in the early stages of rheumatoid arthritis)
C-reactive protein (nonspecific test is used to detect generalized inflammation)
Complement
CBC (number of white blood cells, red blood cells, and platelets present in a sample of blood)
Creatinine (commonly used to diagnose and monitor kidney disease in patients who have a rheumatic condition)
ESR (used to detect inflammation in the body)
Hematocrit (test for hemoglobin concentration and the number of red blood cells present in a sample of blood)
RF

368
Q

ANA tests for _____

A 
RA
SLE
Sjogren syndrome
Scleroderma (diffuse and limited)
Polymyositis and dermatomyositis
369
Q

Anti-native DNA tests for ____

A

SLE

370
Q

RF tests for ___

A 
RA
Sjogren syndrome
Scleroderma
Polymyositis
Dermatomyositis
371
Q

Anti-SM tests for

A

SLE

372
Q

Anti-SS-A tests for

A

Sjogren syndrome

373
Q

Anti SS-B tests for

A

Sjogren syndrome

374
Q

Anti-SCL 70 tests for

A

Scleroderma (diffuse and limited)

375
Q

Anti-Centromere tests for

A

Limited scleroderma

376
Q

Anti-Jo 1 tests for

A

Polymyositis and dermatomyositis

377
Q

General indications for referring a patient for a synovial fluid aspiration (arthrocentesis) and analysis

A

acute arthritis (sepsis, crystal arthritis, and hemorrhagic [trauma]) and chronic arthritis (inflammatory [crystal arthritis, rheumatoid arthritis, spondylarthritis] and noninflammatory [osteoarthritis, osteonecrosis]).

378
Q

_____ is Performed in any patient who presents with a painful joint or joints and evidence of effusion of unknown causes.

A

synovial fluid aspiration (arthrocentesis) and analysis

379
Q

classic early symptomatology observed in a classic patient with Adult RA including joint and constitutional symptoms.

A

Morning stiffness lasting for at least 30 minutes for 6 weeks
Arthritis is proximal smaller joints of hands and feet
Rheumatoid nodules
Ocular symptoms

380
Q

Which joints can be affected by Adult RA, but which are most commonly initially affected?

A

PIP joints of fingers, MCP joints of wrists, knees, ankles, and MTP joints involved
Proximal small joints of hands and feet are effected initially

381
Q

What are common hematologic findings seen in Adult RA?

A

Normocytic hypochromic anemia with low ferritin
WBC usually normal maybe slightly elevated
Platelet count may be slightly elevated in proportion to level of inflammation

382
Q

What is the most useful serologic diagnostic test in Adult RA?

A

Rheumatoid Factor and anti-CCP

383
Q

pros and cons of ordering RF instead of Anti-CCP

A

70-80% of patients w/ RA have sensitivities of only 50% towards RF and anti-CCP tests in early stages

384
Q

pros and cons of ordering RF instead of Anti-CCP

A

Anti-CCP used in conjunction with RF to increase sensitivity and specificity. About 60% sensitive and 99% specific.

385
Q

pros and cons of ordering RF instead of Anti-CCP

A

Anti-CCP is the most specific blood test for RA.
RF can occur in other autoimmune diseases, and is about 80% sensitive and 60% specific. Present in 85% of patients with RA

386
Q

What age, gender, and ethnicity is the most common for a patient with SLE?

A

Young (15-40yo), female – male ratio is 5:1, and blacks 1:250 vs. whites 1:1000

387
Q

What constitutional symptoms are most common in a patient with SLE?

A

Fever, anorexia, weight loss, or malaise

388
Q

What epithelial symptoms are most common in a patient with SLE?

A

Skin rash where exposed to light (face neck, upper chest)
Malar rash, discoid rash, or photosensitivity of skin rashes
Oral ulceration

389
Q

Which organ is most commonly affected by SLE?

A

Kidneys

390
Q

What joints are most commonly affected in SLE?

A

Small joints of hands, wrists, knees

Characterized by tenderness, swelling, or effusion

391
Q

What are the common hematologic changes observed in SLE?

A

Hemolytic anemia, leukopenia, lymphocytopenia, and thrombocytopenia

392
Q
  1. What are the earliest urinary findings observed in SLE?
A 
Persistent proteinuria (>0.5mg/day)
Cellular casts (red, hemoglobin, granular, tubular, or mixed)
393
Q
  1. What serologic test results are commonly observed in SLE?
A

ANA (95-100%) – very specific but not very commonly found in patients w/ SLE
Anti-native DNA (~50%)
Ant-SM (~20%)

394
Q
  1. Briefly describe the different clinical features of Limited Scleroderma
A

Limited: is only limited to the face and hands and is aka as CREST

395
Q

“CREST” for limited scleroderma stands for…

A

Calcium deposits form under skin on fingers
Raynaud’s phenomenon = spasm of blood vessels in fingers/toes in response to cold or stress (turn blue)
Esophageal dysfunction = esophageal dysmotility d/t fibrosis caused by GI hypomotility
Sclerodactyly = tightening of skin causing fingers to bend (d/t CT deposits in subcutaneous tissue)
Telangiectasia = dilated vessels on skin of fingers, face, or inside of mouth

396
Q

Briefly describe the different clinical features of Diffuse Scleroderma

A

Diffuse: is found in other regions of the body
Skin involvement now involves trunk and proximal extremities
More widespread organ involvement (kidney & heart & lung)
GI hypomotility still present d/t fibrosis leading to atrophy of GI tract

397
Q
  1. Which organ system is most commonly affected with Systemic Sclerosis?
A

GI

398
Q
  1. What serologic test is highly specific for SS, but is only positive in 30% of effected patients?
A

Anti-scleroderma antibody (Scl-70)
Present in 30% patients w/ diffuse and only 20%w/ CREST
ANA (80-95%)
Anti-centromere antibody present in 50% of CREST patients (highly specific for limited scleroderma)

399
Q

Describe the classic muscular symptomatology observed in Polymyositis?

A

Gradual and progressive bilateral muscle weakness in proximal upper and lower extremity and neck flexor muscles
Leg weakness proceeds upper extremity involvement
Pain and tenderness present ~25% of time but rarely CC
Muscle atrophy and contracture occurs later
Elevated levels of CK-MB (w/o myocarditis) and AST and ALT are also elevated

400
Q

Elevated levels of CK-MB (w/o myocarditis) and AST and ALT are also elevated with ______

A

polymyositis

401
Q

Describe the classic dermatologic manifestations observed in Dermatomyositis?

A

Rash over butterfly area of face, neck, shoulders, and upper chest/back area

Muscle involvement from polymyositis PLUS dermatologic manifestations

Periorbital edema w/ purplish coloring over eyelids
Hands have scaly patches on dorsum of PIP and MCP joints, papules over knuckles, and erythema under nails

402
Q
  1. What serum chemistry test may be helpful in the diagnosis of Polymyositis and Dermatomyositis?
A

Serum level of the muscle enzymes CK and Aldolase are elevated

403
Q
  1. Elements of which conditions may be observed in a patient with Mixed Connective Tissue Disease (MCTD)?
A

Elements of SLE, PSS, and inflammatory myopathy

404
Q
  1. What is the other name for Mixed Connective Tissue Disease MCTD?
A

SLE w/ minimal renal involvement

405
Q
  1. Describe the classic clinical signs and symptoms observed in a patient with Sjogren’s syndrome.
A 
Everything DRY!
Keratoconjuctivitis (dry eyes)
Xerostomia (dry mouth)
Enlarged parotid gland
Loss of taste or smell
Desiccation of nose, throat, larynx, bronchi, vagina, and skin
406
Q
  1. List the common extra-articular clinical manifestations of Sjogren Syndrome.
A

Dysphagia, vasculitis, pleuritis, obstructive lung disease, neuropsychiatric dysfunction (peripheral neuropathies), pancreatitis, and nephritis

407
Q
  1. Compare and contrast Primary vs. Secondary Sjogren
A

Primary involves salivary, lacrimal, and labial glands. Possible multi-organ involvement
Secondary involves components from primary AND components of RA and SLE (not always called secondary)

408
Q
  1. List the serologic tests available for the diagnosis of Sjogren
A 
Hematology: Mild anemia w/ leukopenia and eosinophilia 
Serology: 
ANA (95%)
Anti-SSB (65%) 
Anti-SSA (65%)
RF (75%)
409
Q
  1. What is the pathologic lesion seen in Temporal Arteritis (AKA Giant Cell Arteritis)?
A

Granulomatous inflammation that disrupts the internal elastic membrane of medium and/or large sized arteries (frequently affects branches of aorta)

410
Q
  1. Describe the classic clinical symptomatology in Temporal Arteritis.
A

Headaches with or without tender or nodular feeling temporal arteries
Visual disturbances
Scalp tenderness
Weight loss
Jaw claudication (highest positive predictive value)
Myalgias and arthralgias

411
Q
  1. What routine laboratory test is most useful in the diagnosis of Temporal Arteritis?
A

ESR > 50mm/h, often > 100mm/h but can also be low or even normal
C-reactive protein slightly more sensitive, normal levels in patients have been described
Mild normochromic and normocytic anemia w/ thrombocytosis
ALP elevated in 20% of patients

412
Q
  1. Describe the classic symptomatology in Polymyalgia Rheumatica (PMR).
A

Pain and stiffness in proximal limb girdle joints and lower back
Often accompanied by fever, malaise, and weight loss
2/3 patients have PMR w/o GCA

413
Q
  1. What routine laboratory test is most useful in the diagnosis of PMR?
A

CBC (to test for anemia)

Elevated acute phase reactants (marked elevation of ESR)

414
Q
  1. What are the most common host factors seen in Ankylosing Spondylitis (AS)?
A

Male>female, Caucasian>African Americans, and age between 20-40 years old

415
Q
  1. Describe the typical onset symptomatology observed in AS?
A

Sacroiliitis is hallmark feature
Bouts of low back pain beginning in late adolescence or early adulthood
Pain and stiffness that is worse with prolonged inactivity (worse in morning)
Pain and stiffness improve with activity
Progressive loss of motion in back, progress cephalad
Lumbar curve flattened and thoracic curve exaggerated
Entire spine becomes fused
May lead to radicular pain syndrome and involve peripheral joints
Inflammatory eye problems common

416
Q
  1. *Be able to explain why most asymptomatic people with a positive HLA-B27 do not have AS.
A

Highly sensitive test (not specific)

417
Q
  1. Reiter’s Syndrome is also called Reactive Arthritis. What is it “reactive” to?
A

Reacts to infections from genitourinary or gastrointestinal tract
Infections from dysentery or STI

418
Q
  1. What are the three classic clinical manifestations of Reiter’s?
A

Conjunctivitis: occurs at same time or few days after onset (Eyes infection)
Urethritis: occurs first, dysuria and mucopurulent discharge present (Urethra infection)
Arthritis: follows 1-4 weeks after infection, asymmetric and affects larger weight bearing joints (Joint infection)
Joints appear to be septic but are sterile (knees, ankles, elbow, or SI)

419
Q
  1. What is the name of the classic rash that appears on the feet of a patient with Reiter
A

Keratoderma blennorrhagicum, is a maculopapular rash

420
Q
  1. Are there any good routine laboratory tests worth ordering if you suspect a patient of having Reiter’s?
A

Nothing specific, positive HLA-B27 in 85% and elevated ESR in 70% of patients

421
Q
  1. 5-7% of patients with psoriasis develop what form of arthritis?
A 
Psoriatic arthritis
Symmetric polyarthtis resembling RA but w/ fewer joints
Arthritis mutilans (derangement of any joint ) and marked osteolysis (active resorption of bone matrix by osteoclasts during the natural formation of health bones)
422
Q
  1. Patients with a history of inflammatory bowel disease are at risk for developing either a peripheral or spondylitic form of arthritis. What are the two most common bowel diseases implicated in this arthritis, and which surgery predisposes an individual for this arthritis?
A

Crohn’s disease and Ulcerative Colitis
Post-jejunoileal bypass surgery
(+) RF and ANA

423
Q
  1. A patient’s synovial fluid must be supersaturated with monosodium urate (uric acid) in order to have gout?
A

Hyperuricemic body fluids

424
Q
  1. Decreased ____of uric acid, or increased ____can result in hyperuricemia.
A

renal clearance & purine synthesis

425
Q
  1. Do all people with hyperuricemia develop gout?
A

No, the greater the degree and duration of hyperuricemia, the greater the chance of crystal deposition and of acute attacks of gout

426
Q
  1. Describe a classic initial episode of Podagra.
A

First acute attack usually occurs at night in MP joint of big toe. Joint is swollen, exquisitely tender, with the overlying skin appearing tense and dusky red

427
Q
  1. Does a normal serum uric acid absolutely rule out gout in a patient with a gouty-appearing joint?
A

No! Clinical presentation can be sufficient for diagnosis, monitor

428
Q
  1. What joints besides the big toe are commonly involved in gout?
A

Hands, feet, and prepatellar bursas

429
Q
  1. What are four abnormal host factors associated with Nongonococcal septic arthritis?
A

Patient experiences sudden acute pain, swelling, and heat at infected joint (80% of time) and possible fever/chills
Most often seen in large weight bearing joints and wrists
IV drug users
Immunocompromised
Joints damaged by other diseases such as RA
Recent prosthetic or arthroscopic surgical procedures

430
Q
  1. Other than a purulent monoarthritis (pus seen in knee, wrist, ankle, or elbow), how else can Gonococcal Septic Arthritis manifest itself?
A

Tenosynovitis (inflammation of the fluid-filled sheath) of wrists, fingers, ankles or toes
Hosts are typically healthy, women>men, rare after 40 years old, and common in homosexual males

431
Q
  1. What is the most valuable diagnostic laboratory test used in septic arthritis?
A

Synovial fluid analysis

432
Q
  1. What is the causative agent of Lyme disease?
A

Lxodes (deer) tick, spreads the infection of Borrelia Bugdorferi

433
Q

Stages of Lyme disease.

A

Stage 1 = early localized infection
Stage 2 = early disseminated infection
Stage 3 = late persistent infection

434
Q

S/S Stage 1 Lyme dz= early localized infection

A
  • After 3-32 day incubation period (7-10 day average), classic rash called erythema migrans forms and last 3-4 weeks
  • Accompanied by a flu like fever, chills, fatigue, malaise, headache, myalgias, and arthralgias
  • Asymptomatic (no rash or flu) is possible
435
Q

S/S Stage 2 Lyme dz= early disseminated infection

A

Weeks – months after inoculation, hematogenous and lymphatic spread
Fatigue and malaise persistent
Skin: smaller popular lesions, not a bite site
CNS: aseptic meningitis, encephalitis, Bell’s palsy, headache, and mood swings/irritability/personality changes
Musculoskeletal: migratory pains in joints muscles and tendons that is intermittent
Cardiac: myocarditis, pericarditis, arrhythmias, and heart block

436
Q

S/S Stage 3 Lyme’s Dz= late persistent infection

A

-Occurs months to years after initial infection and may not be preceded by apparent stage 1 or 2
-Musculoskeletal: joint and periarticular pain similar to or perhaps fibromyalgia, chronic/recurrent large joint arthritis, and chronic (possibly debilitating) synovitis
-Neurologic: subacute encephalopathy (memory loss, mood changes, sleep disturbances, and axonal polyneuropathies)
-Skin: acrodermatitis chronicum atrophians
Atrophy of the skin, skin begins to wrinkle

437
Q
  1. Although the result may be negative in stage I, what test should be run if you suspect Lyme disease?
A

Serologic test=

  • ELISA
  • Then confirmed with a Western immunoblot assay that can detect both IgM and IgG antibodies (often negative in first stage)
  • Acute and convalescent titers should be obtained in early stages
438
Q

Lyme’s Dz Test called Western immunoblot assay that can detect _____ antibodies

A
  • BOTH IgM and IgG antibodies (often negative in first stage)
  • IgM appears first 2-4 weeks after onset of EM, and peaks at 6-8 weeks, and then declines after 4-6 months
  • IgG occurs later (6-8 weeks) and peaks at 4-6 months
439
Q
  1. What test may be valuable to order if you suspect stages II or Ill Lyme disease?
A

Two stage testing w/ ELISA and Western Blot

440
Q
  1. What is Acute Rheumatic Fever (ARF)?
A
  • Systemic immune response following 0.3% of cases of infectious pharyngitis w/ group A beta-hemolytic Strep.
  • Causes focal perivascular granulomatous reaction w/ vasculitis
  • inflammatory reaction in various tissues , necrosis of collagen
441
Q
  1. What are the six most common clinical manifestations observed in ARF?
A 
Carditis
Erythema marginatum
Subcutaneous nodules
Sydenham’s chorea
Polyarthrtisis
Minor signs
442
Q

ARF Cardio S/S…

A 
Pericarditis
Cardiomegaly
Congestive heart failure
Mitral or aortic regurgitation murmurs
ECG changes
Altered heart sounds
Arrhythmias
443
Q

ARF Erythema marginatum S/S…

A

EM are rapidly enlarging macules that change into rings w/ a clear center

444
Q

Acute Rheumatic Fever (ARF) Subcutaneous nodules S/S…

A

Are small firm and are attached to fascia or tendon overlying bony promeninces, lasts for days or weeks and recur

445
Q

Acute Rheumatic Fever (ARF) Sydenham’s chorea S/S…

A

Involuntary movement disorder of the face, tongue, and upper extremities

446
Q

ARF Polyarthrtisis S/S…

A

Migratory in nature and involve large joints

447
Q

ARF Minor signs S/S…

A 
Fever
Polyarthralgias
Reversible prolonged PR interval
Rapid sedimentation rate or positive CRP
Evidence of antecedent Beta-hemolytic strep infection
448
Q
  1. Is a throat culture necessary to diagnosis ARF?
A

No, they are often negative one ARF is suspected

A positive throat culture does not rule in ARF nor does a negative culture rule out ARF

449
Q
  1. What serologic test is helpful in the diagnosis of ARF?
A

ESR and CRP

Antistreptolysin-O test or Anti-DNAse B

450
Q

Etiology of benign prostatic hyperplasia (BPH)…

A

Not totally understood,

Endocrinologic – dihydrotestosterone

451
Q

Epidemiology of BPH…

A

Incidence increased with age (50% ^ with 6th decade of life)

452
Q

Clinical symptomatology of benign prostatic hyperplasia (BPH)…

A 
Obstructive= Hesitancy, Decreased force and caliber of urinary stream, Sensation of incomplete bladder emptying, Double voiding, Straining to urinate, Postvoid dribble
Irritative= Urgency increased, Frequency increased, Nocturia more common
453
Q

Describe the role of the laboratory in BPH

A

Urinalysis to r/o infection
Serum PSA to help r/o cancer
Seam creatinine to asses renal function

454
Q
  1. Know the important epidemiologic facts associated with prostate cancer
A

Diet (rich in fatty foods), family history, and people of Black descent
Highest incidence in north America and Europe

455
Q
  1. Lists the methods available for detecting prostate cancer…
A

PSA
DRE
TRUS
TRUS guided biopsy

456
Q

PSA for detecting prostate cancer…

A

Serum levels correlate with volume of bone benign and malignant prostatic tissues
Useful in detecting staging of disease, monitoring response to treatment, and detecting reoccurrence
Goal is enhanced sensitivity (increase cancer detection) and specificity (eliminate costly/invasive prostate biopsies that show normal results)

457
Q

DRE for detecting prostate cancer…

A

Detects 1.5-7% of cancers in stage T3 or greater

Not a good indicator of prostate cancer

458
Q

TRUS for detecting prostate cancer…

A

Should not be used as first line screening tool
Lacks specificity
Detection rate of significant cancers not much better than a combination of PSA and DRE

459
Q

TRUS guided biopsy for detecting prostate cancer…

A

Final diagnosis

Goal of previous tests is to determine who gets biopsied

460
Q

PSA velocity (PSAV)

A 
PSA velocity (PSAV)establishes rate of increased serum PSA per year
 >0.75ng/mL/year increases likelihood of cancer
461
Q

PSA density (PSAD)

A 
PSA density (PSAD) is the ratio of serum PSA concentration and prostate volume as determined by TRUS
Used when patient has elevated PSA yet DRE and TRUS are normal
462
Q

Molecular forms of PSA

A

Complexed (protein bound) PSA
Complex PSA is produced by malignant cells
Free PSA (f-PSA) = value established as % free PSA
Malignant cells produce less than normal amounts of free PSA

463
Q

Men __ years old with a family history of prostate cancer undergo annual prostatic evaluation of both DRE and serum PSA yearly

A

40yr

464
Q

Recommended that baseline PSA and DRE be offered to men as young as _ w/ a life expectancy of _ years or more

A

40yr & 10yr

465
Q

PSA value below which a man may be reassured that he does not have biopsy-detectable prostate cancer?

A

NONE

466
Q

Men __ years or older undergo an annual prostatic evaluation consisting of both DRE and serum PSA

A

50 yr

467
Q
  1. Be able to intelligibly discuss the basis for the controversy that exists in routinely screening for prostate cancer
A

PSA and DRE can produce false positives and false negatives
Abnormal results from screening with PSA and DRE require prostate biopsies which can be painful and lead to complications like infection or bleeding

468
Q
  1. List the important epidemiologic features of Renal Cell Carcinoma
A

Smoking tobacco (cigarette smoking)

469
Q
  1. List the common symptoms observed in a patient with Renal Cell Carcinoma
A

Flank pain, abdominal mass/pain, systemic symptoms (fever, night sweats, weight loss, or malaise), hematuria, metastatic disease (cough or bone pain) and solid renal mass on imaging

470
Q
  1. List the common laboratory changes observed in a patient with Renal Cell Carcinoma
A
  • Increased alkaline phosphatase; Only if bony metastasis
  • Hypercalcemia; Big deal! d/t parathyroid disease or cancer
  • Hematuria; Unexplained PAINLESS, only lab finding indicative of renal cell carcinoma
  • Anemia; D/t decrease production of EPO by KD cells
  • Erythrocytosis possible; Cancer cells can start producing EPO and cause increase in # RBC
471
Q

Three phases/components of clot formation =

A

Vasoconstriction
Platelet plug formation
Coagulation

472
Q

Platelet plug formation Tests

A 
Platelet count – measures total number of platelets in blood, determined by a routine CBC
Bleeding Time (BT) –used as a platelet function test, evaluates interaction of platelets with vessel wall and the formation of a plug; test is independent on coagulation.
473
Q

Prolonged/increased bleeding time d/t

A

decreased platelet count or abnormal platelets causes plug not to form
Platelet count test must be done first to ensure that platelets are present before testing the function of platelets

474
Q

Coagulation Tests

A

Prothrombin Time (PT) – time it takes plasma specimen to yield a fibrin clot once extrinsic pathway is initiated

(Activated) Partial Thromboplastin Time (APTT or PTT) – time it takes a plasma specimen to yield a fibrin clot once intrinsic pathway is initiated

475
Q

Coagulation Prothrombin Time (PT) –

A

A good screening test for extrinsic pathway function (sensitive but not specific)
Any deficiency in extrinsic pathway will prolong the test
Helpful for monitoring patients on therapeutic coumarin

476
Q

Coagulation Activated Partial Thromboplastin Time (APTT or PTT) –

A

A good screening test for intrinsic pathway function (sensitive but not specific)
Any deficiency in intrinsic pathway will prolong the test
Helpful for monitoring patients on therapeutic heparin

477
Q
  1. Briefly describe the process of fibrinolysis; know the name and rationale of the test used for evaluation of this process
A

Fibrinolysis is the degradation of the fibrin clot formed during clot formation. It involves fibrin-specific plasminogen activators to activate plasminogen into plasmin, which then degrades the fibrin in fibrin degradation products.

478
Q

Test fibrinolysis with

A

Prothrombin Time (PT) or the (Activated) Partial Thromboplastin Time (APTT)

479
Q

Platelet Count

A

part of a routine CBC, tests totally number of platelets in circulation

480
Q

Bleeding Time (BT) –

A

platelet function test, tests interaction of platelets and vessel wall. BT will increase with a decreased platelet count (even when they are ALL properly functioning)

481
Q

Prothrombin Time (PT) –

A

time it takes to yield a fibrin clot once the extrinsic pathway is initiated; monitors patients on therapeutic coumarin

482
Q

Activated Partial Thromboplastin Time (APTT) –

A

time it takes to yield a clot once the intrinsic pathway is initiated; monitors patients on therapeutic heparin

483
Q

Prolonged tests for competency of hemostasis:

A

BT: Liver cirrhosis and von WIllebrand’s disease
PT: Liver cirrhosis, early hepatic insufficiency, and vitamin K deficiency
APTT: Liver cirrhosis and hemophilia A

484
Q

Tests used to screen for the competency of hemostasis

A 
Platelet Count
Bleeding Time (BT)
Prothrombin Time (PT) 
Activated Partial Thromboplastin Time (APTT)
Prolonged tests
485
Q
  1. Name the factor deficient in hemophilia A
A

Factor VIII  causes bleeding into joints

486
Q
  1. Name the factor deficient in hemophilia B
A

Factor IX

487
Q
  1. Name the factor deficient in Von Willebrand’s disease
A

Deficient or dysfunctional von Willebrand’s factor  vW factor is essential in mediation of platelet adhesion and preserves VIII:C from degradation

488
Q
  1. Name four basic causes of Vit K associated with bleeding problems
A

-Nutritional deficit  rare

-Malabsorptive syndrome=
…Broad spectrum antibiotics  destroys endogenous GI flora which normally makes body’s vitamin K
…Biliary tract disease  bile is important in fat emulsification and absorption

-Vitamin K antagonistic medicine  not a true deficiency, just impairs vitamin K’s role

489
Q
  1. Name the test used to periodically monitor the use of Warfarin anticoagulants
A

International Normalized Ratio (INR)

490
Q
  1. List seven causes of thrombocytopenia due to bone marrow suppression
A 
Aplastic anemia
Leukemias
Metastatic lymphoma or carcinoma replacing bone marrow
Folic acid or vitamin B12 deficiencies
Chemotherapy and radiation therapy
Viral infections (HIV, HBV, EBV, or CMV)
Drugs
491
Q
  1. Give a basic definition of idiopathic thrombocytopenic purpura
A

Autoimmune response where IgG antibodies coat platelets (recognizes them as foreign) resulting in splenic sequestration of the platelets where they are destroyed (no splenomegaly)

492
Q

Describe two forms of idiopathic thrombocytopenic purpura

A

Acute
Pediatric, abrupt onset, 80% are d/t post viral infection, short clinical course with reduced platelet counts with spontaneous remissions, and Tx is supportative

Chronic
Adult, insidious onset associated w/ other systemic diseases (but rarely with viral infections), longer clinical course (years in duration) with it rarely spontaneous remising, and Tx via corticosteroids or splenectomy.

Clin Path Final Q7 (1 decks)

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