Nycc Dr Wells Lab Diagnosis Exam 3

Front 1

Proteinuria

Back 1

Long distance athletes:
ALL proteinuria MUST be explained

Front 2

Proteinuria is the first indication of kidney disease when

Back 2

it's NOT benign.

Means glomeruli/tubules are leaking. Serum proteins reabsorbed, and it's presence means lack of absorption or impaired filtration

Front 3

TIME necessary to collect proteinuria test?

Back 3

24 hours

Front 4

Benign proteinuria

Back 4

be/c you loose water, therefore makes protein LOOK higher
Due to:
1. Dehydration
2. Strenuous exercise
3. Fever
4. Acute non-renal illness
5. Orthostatic postural proteinuria

Front 5

Proteinuria is defined as greater than

Back 5

>150 mg per day

Front 6

Transient proteinuria

Back 6

goes away

2+ protein, the dipstick test should be done on a MORNING specimen 2x in the next month.
If subsequent dipstick results are negative, the patient has transient proteinuria.

Front 7

Orthostatic proteinuria

Back 7

Secondary to body position
Persons younger than 30 who excrete LESS than 2g of protein per day and have normal creatinine clearance should be tested for OP

Front 8

Orthostatic proteinuria characterized by

Back 8

increased protein excretion in the UPRIGHT position, but normal when supine

Front 9

Proteinuria is always BAD when

Back 9

> 4.0 grams

ALWAYS GLOMERULAR

Front 10

What kind of people with proteinuria will chiros see?

Back 10

ELITE athletes
SLE patients w/ secondary glomerulonephritis WITHOUT kidney dz.
Diabetes (kidney damage)
Multiple Myeloma = Bence Jones protein
Elite Athletes

Front 11

Normally there is some daily RBC excretion into urine (0-5 RBCs) but what level indicates TROUBLE?

5 TICS

Back 11

>5 RBC's = TICS

= trauma, infection (pyleo/bladder), cancer, stones

Front 12

How to measure hematuria?

Back 12

DIPSTICK test measures presence of HEMOGLOBIN in urine, the MICRO exam detects RBC

Front 13

Hemoglobinuria

Back 13

increase in intact RBC's
OR
lysed RBC's in urine

Front 14

Hematuria

Back 14

increase in intact RBC's in urine, only

Front 15

Intravascular hemolysis

Back 15

hemoglobin positive but NO intact RBC's

Front 16

RBC CASTS

Back 16

no, not the cast of a soap opera...
often found in glomerular diseases**** along with > 4.0 grams of proteins)

Front 17

What are simple cystitis sx

Back 17

Dysuria (painful urination)
Urgency
Some hematuria
Frequency
Oliguria (not much there)
Nocturia (nighttime urine)
Suprapubic pain (wayyyy south)

Front 18

tx for cystitis

Back 18

sulfa drugs

(pyridoxine - not test question. Turns urine bright orange)

Front 19

RBC casts are indicative of

Back 19

GLOMERULONEPHRITIS

Front 20

Pyuria sx

Back 20

>5 WBC's

Front 21

WBC's without bacteria

Back 21

RENAL CALCULI (or tubulointerstitial) or Prostatitis

Front 22

Negative nitrite

Back 22

YEASTS and some Gram (+) cocci do not reduce nitrates to nitrites

Front 23

Increased WBC's and bacteria

Back 23

UTI

Front 24

Bacteria WITHOUT increase in WBC's

Back 24

random urine sample, normal contamination with flora

Front 25

WBC's without bacteria - look under scope

Back 25

Prostatitis -leaks WBC's into urine

Front 26

UTI patients

Back 26

females
Adult women in late teens
NO fever, NO low back pain
Dysuria
Increased frequency and urgency
Nocturia
IF LBP and blood - could be raging bladder infection

Front 27

RIsk of UTI remaining untreated

Back 27

Pyelonephritis

Back pain at CV angle, FEVER, chills, nausea, vomiting =sick

Front 28

Bilirubinuria

Back 28

Bilirubin in urine:

LIVER dysfunction = unconjugated bilirubin/indirect
or
BILIARY obstruction w/ large amts of conjugated/direct bilirubin entering bloodstream b/c liver is fine

Front 29

Urinary urobilogen

Back 29

Formed by DEGREDATION of bilirubin (by bacteria in intestines)

Almost 50% is reabsorbed by the liver, and some by kidneys so INCREASED urobilinogen indicates LIVER DISEASE or HEMOLYTIC anemia.

Front 30

Does biliary obstruction increase urobilinogen?

Back 30

NO!!!!

(bile duct obstruction)

Front 31

Ketonuria

Back 31

urinary ketones appear in patients w/ poorly controlled DM

Starvation /decrease intake of carbs/ prolonged vomiting

Front 32

Glucosuria

Back 32

monitor patients w/ DM

Renal threshold for glucose is 180 mg/dl

Front 33

PLASMA PROTEINS are produced in the _______

Back 33

LIVER

*sick liver, no plasma proteins

Front 34

Plasma proteins are present in serum and plasma, except ______

Back 34

fibrinogen

Front 35

Exceptions of peptide hormones NOT produced in liver

Back 35

von Willebrand factor (8)
Immunoglobulins

Front 36

Which serum protein would be elevated during an iMMune reaction?

Back 36

gaMMa***

Front 37

Functions of plasma proteins

Back 37

transport (albumin, liproproteins)
protect from inflammation (gammaglobulins)
osmotic pressure maintenance (albumin)**
Negative Nitrogen balance for protein catabolism
Positive Nitrogen balance for synthesis of proteins

Front 38

Protein catabolism
AA > deamination > _____ > _____ > _____ ________
AA > deamination > ______> _______> _______

Back 38

NH3 > urea cycle > urea

Ketoacids > citric acid cycle > Fat/Glucose

Front 39

Proteins that modify inflammatory response

Back 39

***ACUTE PHASE REACTANTS***

some are pos some are neg but in lab can fool us because patient is sick with something else that caused acute phase reactant levels to change

Front 40

Most proteins produced in liver are from dietary AA's. What leads to decreased levels of plasma proteins?

Back 40

LIVER DISEASE
&
PROTEIN MALNUTRITION

Front 41

Cytokines (IL-1 and IL-6) stimulate hepatic synthesis of

Back 41

ACUTE PHASE REACTANTS - proteins that MODIFY the inflammatory response

(+) acute phase reaction
(-) acute phase reaction

Front 42

If you are sick, do you have lower or higher acute phase reactants

Back 42

higher if inflammatory
except...

Synthesis of some transport proteins (albumin and transferrin) are LOWER because they are inhibited by acute phase reactants

Front 43

Protein analysis provides information on

Back 43

nutritional status

severe disease states of liver, kidney, bone marrow

Front 44

Provides clues to the presence of abnormal proteins

Back 44

Serum electrophoresis

Front 45

Albumin is bigger than

Back 45

globulin

If ratio reversed, [A/G] then maybe multiple myeloma of plasma cells kicking out abnormal globulins so inversed A/G ratio

Front 46

It is a type of electrolyte disturbance. In the blood, about half of all calcium is bound to proteins such as serum albumin, but it is the unbound, or ionized,

Back 46

HYPOcalcemia

Front 47

It manifests as a symptom of a parathyroid hormone [PTH] deficiency/malfunction, a Vitamin D deficiency, or unusually high magnesium levels hypermagnesaemia, or low magnesium levels hypomagnesaemia.

Back 47

HYPOcalcemia

Front 48

may be associated with low PTH levels as seen in hereditary hypoparathyroidism, acquired hypoparathyroidism (surgical removal MCC of hypoparathyroidism), and hypomagnesaemia.

Back 48

HYPOcalcemia

Front 49

explain why HIGH PTH levels are created by low calcium levels

Back 49

INEFFECTIVE PTH : associated with high PTH levels when the parathyroid hormone is ineffective; in chronic renal failure, the hydroxylation of vitamin D is ineffective, calcium levels in the blood fall, and high PTH levels are produced in response to the low calcium, but fail to return calcium levels to normal.

Front 50

HYPOcalcemia created by ABSENT parathyroid hormone (how would this happen?)

Back 50

Following thyroidectomy, the parathyroid glands are located very close to the thyroid and are easily injured or even accidentally removed during thyroidectomy

Front 51

Patient presentation of hypocalcemia

Back 51

Petechia which appear as on-off spots, then later become confluent, and appear as purpura (larger bruised areas, usually in dependent regions of the body).
Oral, perioral and acral paresthesias, tingling or 'pins and needles' sensation in and around the mouth and lips, and in the extremities of the hands and feet. This is often the earliest symptom of hypocalcaemia.
Carpopedal and generalized tetany (medical sign), (unrelieved and strong contractions of the hands, and in the large muscles of the rest of the body) are seen.
Latent tetany

Front 52

Chvostek's sign (tapping of the inferior portion of the zygoma will produce facial spasms)

Back 52

hypocalcemia

Front 53

Hypocalcemia alkalosis as it relates to albumin

Back 53

As blood plasma hydrogen ion concentration decreases, caused by respiratory or metabolic alkalosis, freely ionized calcium concentration decreases. This freely ionized calcium is the biologically active component of blood calcium. Since a portion of both hydrogen ions and calcium are bound to serum albumin, when blood becomes alkalotic, bound hydrogen ions dissociate from albumin, freeing up the albumin to bind with more calcium and thereby decreasing the freely ionized portion of total serum calcium.

Front 54

related to alkalosis is partially responsible for the cerebral vasoconstriction that causes the lightheadedness, fainting, and paraesthesia often seen with hyperventilation. Tetany may also be seen with this condition.

Back 54

hypocalcemia

Front 55

simply put, what can cause hypERcalcemia?

Back 55

It can be due to excessive skeletal calcium release, increased intestinal calcium absorption, or decreased renal calcium excretion.

Front 56

mnemonic for hypERcalcemia

Back 56

There is a general mnemonic for remembering the effects of Hypercalcaemia: "Stones, Bones, Groans, Thrones and Psychiatric Overtones"

-Stones (renal or biliary)
-Bones (bone pain)
-Groans (abdominal pain, nausea and vomiting)
-Thrones (sit on throne - [polyuria])
-Psychiatric overtones (Depression 30-40%, anxiety, cognitive dysfunction, coma)

Front 57

account for about 90% of cases of hypercalcaemia.

Back 57

Primary hyperparathyroidism and malignancy

Front 58

other causes of hypERcalcemia besides primary hyperparathyroidism (90%)

Back 58

haematologic malignancy (multiple myeloma, lymphoma, leukaemia)

Front 59

Decreased intestinal magnesium reabsorption and the resulting decrease in serum magnesium levels is believed to cause lowered parathyroid hormone (PTH) output by the parathyroid gland.

Back 59

This results in decreased PTH and decreased serum calcium levels (hypocalcemia)

Front 60

Ten to twenty percent of all hospital patients and 60–65% of patient in the intensive care unit (ICU) have hypomagnesemia.

Back 60

Low levels of magnesium in blood may mean that there is not enough magnesium in the diet, the intestines are not absorbing enough magnesium, or the kidneys are excreting too much magnesium

Front 61

Alcoholism and hyPOmagnesmia

Back 61

Alcoholism. Hypomagnesemia occurs in 30% of alcohol abuse and 85% in delirium tremens, due to malnutrition and chronic diarrhea. Alcohol stimulates renal excretion of magnesium, which is also increased because of alcoholic and diabetic ketoacidosis, hypophosphatemia and hyperaldosteronism resulting from liver disease. Also, hypomagnesemia is related to thiamine deficiency because magnesium is needed for transforming thiamine into thiamine pyrophosphate.

Front 62

P.R.O.F. BoT has HIGH Alk Phos

Back 62

Pagets, Rickets, Osteomalacia, Fractures, Bone Tumors
= HIGH alk phos levels

Front 63

a hydrolase enzyme responsible for removing PHOSphate groups from many types of molecules, including nucleotides, proteins, and ALKaloids. The process of removing the phosphate group is called dephosphorylation

Back 63

alkaline phosphatase

Front 64

Where is alk phos found?

Back 64

n humans, alkaline phosphatase is present in all tissues throughout the entire body, but is particularly concentrated in liver, bile duct, kidney, bone, and the placenta.

Front 65

High _____- levels can show that the bile ducts are blocked.

Back 65

ALP

*alkaline phosphatase

Front 66

Levels are significantly higher in children and pregnant women.

Back 66

ALP

Front 67

Also, elevated ALP indicates that there could be active bone formation occurring as ____ is a byproduct of osteoBLAST! activity (such as the case in Paget's disease of bone).

Back 67

ALP

Front 68

Osteoporosis and PTH

Back 68

Mild vitamin D insufficiency is associated with increased Parathyroid Hormone (PTH) production.[14] PTH increases bone resorption, leading to bone loss.

Front 69

Osteoporosis and endocrine fcn

Back 69

Endocrine disorders that can induce bone loss include Cushing's syndrome,[14] hyperparathyroidism,[14] thyrotoxicosis,[14] hypothyroidism, diabetes mellitus type 1 and 2,[33] acromegaly and adrenal insufficiency. In pregnancy and lactation, there can be a reversible bone loss

Front 70

calcium
vitamin D both low

PTH high

causes?

Back 70

n addition to estrogen, calcium metabolism plays a significant role in bone turnover, and deficiency of calcium and vitamin D leads to impaired bone deposition; in addition, the parathyroid glands react to low calcium levels by secreting parathyroid hormone (parathormone, PTH), which increases bone resorption to ensure sufficient calcium in the blood.

Front 71

PTH in the kidney

Back 71

It enhances active reabsorption of calcium and magnesium from distal tubules and the thick ascending limb. As bone is degraded both calcium and phosphate are released. It also decreases the reabsorption of phosphate, with a net loss in plasma phosphate concentration. By increasing the calcium:phosphate ratio more calcium is therefore free in the circulation

Front 72

PTH effect on intestine

Back 72

It enhances the absorption of calcium in the intestine by increasing the production of activated vitamin D. Vitamin D activation occurs in the kidney.

Front 73

A high level of PTH in the blood is known as

Back 73

hyperparathyroidism

Front 74

secondary hyperparathyroidism

Back 74

This can occur in chronic renal failure. In secondary hyperparathyroidism, serum calcium levels are decreased, which causes the hypersecretion of PTH from the parathyroid glands. PTH acts on the proximal tubules in the kidney to decrease reabsorption of phosphate (increasing its excretion in urine, decreasing its serum concentration), but enhances active reabsorption of calcium and magnesium from distal tubules and the thick ascending limb. NOTE: in chronic renal failure, the failing kidneys are unable to excrete phosphate in the urine. In this case of secondary hyperparathyroidism, serum calcium will be decreased, but serum phosphate will be increased.

Front 75

Chronic renal failure and PTH

Back 75

in chronic renal failure, the failing kidneys are unable to excrete phosphate in the urine. In this case of secondary hyperparathyroidism, serum calcium will be decreased, but serum phosphate will be increased.

Front 76

is an electrolyte disturbance in which there is an abnormally low level of phosphate in the blood.

Back 76

Hypophosphatemia

Front 77

refeeding syndrome and hypOphosphatemia

Back 77

but is most commonly seen when malnourished patients (especially chronic alcoholics) are given large amounts of carbohydrates, which creates a high phosphorus demand by cells, removing phosphate from the blood (refeeding syndrome).

Front 78

A decrease in phosphate in the blood is sometimes associated with an increase in phosphate in the

Back 78

URINE

can't absorb it in the intestines and you can't hang on to it in the kidneys

Front 79

Hypophosphatemia is caused by the following three mechanisms:

Back 79

Inadequate intake =(often unmasked in refeeding after long-term low phosphate intake)

Increased excretion = (e.g. in hyperparathyroidism, hypophosphatemic rickets)

Shift from extracellular to intracellular space = (seen in treatment of diabetic ketoacidosis, refeeding, short-term increases in cellular demand (e.g., hungry bones syndrome) and acute respiratory alkalosis)

Front 80

Deficiency results in impaired bone mineralization and leads to bone softening diseases including rickets in children and osteomalacia and osteoporosis in adults.

Back 80

vitamin D

*hypovitaminosis D

Front 81

Prerenal causes of AKI ("pre-renal azotemia") are those that

Back 81

decrease blood flow to kidney

*These include systemic causes, such as low blood volume, low blood pressure, and heart failure, as well as local changes to the blood vessels supplying the kidney. The latter include renal artery stenosis, which is a narrowing of the renal artery that supplies the kidney, and renal vein thrombosis, which is the formation of a blood clot in the renal vein that drains blood from the kidney.

Front 82

Post-renal failure

Back 82

Postrenal AKI is a consequence of urinary tract obstruction. This may be related to benign prostatic hyperplasia, kidney stones, obstructed urinary catheter, bladder stone, bladder, ureteral or renal malignancy. I

Front 83

The deterioration of renal function may be discovered by a measured decrease in urine output. Often, it is diagnosed on the basis of blood tests for substances normally eliminated by the kidney: urea and creatinine. BEST marker of the two?

Back 83

CREATININE

Front 84

Creatinine is not affected by _____, unlike BUN

Back 84

diet

*BUN is protein breakdown

Front 85

overweight people, alcoholics, metabolic syndrome, gout

Back 85

hyperuricemia


Renal underexcretion of uric acid is the primary cause of hyperuricemia in about 90% of cases,

Front 86

tophus made of

Back 86

crystals and white cells

Front 87

HYPERURICEMIA causes

Back 87

Hyperuricemia is the underlying cause of gout. This can occur for a number of reasons, including diet, genetic predisposition, or underexcretion of urate, the salts of uric acid.[2] Renal underexcretion of uric acid is the primary cause of hyperuricemia in about 90% of cases, while overproduction is the cause in less than 10%.[

Front 88

gout lab

Back 88

uric acid
WBC
ESR
=elevated

Front 89

Elevated levels of uric acid in gout patients may lead to crystals precipitating in the kidneys and then?

Back 89

Elevated levels of uric acid may also lead to crystals precipitating in the kidneys, resulting in stone formation and subsequent urate nephropathy.[5]

Front 90

is a rapidly worsening (decreasing) kidney function (renal insufficiency) that is caused by high levels of uric acid in the urine (hyperuricosuria).

Back 90

nephropathy

*assoc. w/ RENAL complications of GOUT:
Nephrolithiasis,
Acute gout nephropathy,
Chronic gouty nephropathy

Front 91

Acute Gouty Nephropathy

Back 91

* cell destruction = lose kidney, need transplant (class)

Wiki: Acute uric acid nephropathy is usually seen as part of the tumor lysis syndrome in patients undergoing chemotherapy or radiation therapy for the treatment of malignancies with rapid cell turnover, such as leukemia and lymphoma. It may also occur in these patients before treatment is begun, due to spontaneous tumor cell lysis (high incidence in Burkitt's lymphoma).

Acute uric acid nephropathy can also be caused by an acute attack of gout.

Front 92

ACUTE Gouty Nephropathy CAUSE

Back 92

caused by deposition of uric acid crystals within the kidney

interstitium and tubules, leading to partial or complete obstruction of collecting ducts, renal pelvis, or ureter. This obstruction is usually bilateral, and patients follow the clinical course of acute renal failure

Front 93

ACUTE gouty nephropathy diagnosis via labs

Back 93

The picture of acute renal failure is observed: decreased urine production and rapidly rising serum creatinine levels. Acute uric acid nephropathy is differentiated from other forms of acute renal failure by the finding of a urine uric acid/creatinine ratio > 1 in a random urine sample.

Front 94

high levels of uric acid in urine

Back 94

hyperuricosuria

*renal complication of gout causing acute gouty nephropathy

Front 95

Urinary stones are typically classified by their location in the kidney (________lithiasis), ureter (ureterolithiasis), or bladder (cystolithiasis), or by their chemical composition (calcium-containing, struvite, uric acid, or other compounds).

Back 95

NEPHRO

Front 96

Ureteral obstruction causes _______-renal azotemia and hydronephrosis (distension and dilation of the renal pelvis and calyces), as well as spasm of the ureter.

Back 96

POSTrenal is a kidney stone in the ureter

Front 97

2 tests for kidney stones (nephrolithiasis)

Back 97

1. complete blood count (CBC), looking for neutrophilia (increased neutrophil granulocyte count) suggestive of bacterial infection, as seen in the setting of struvite stones;

2.renal function tests to look for abnormally high blood calcium blood levels (hypercalcemia);

Front 98

glomerular filtration rate (GFR).

Back 98

The rate at which blood is filtered through all of the glomeruli, and thus the measure of the overall renal function, is the glomerular filtration rate (GFR).

Front 99

Creatinine, for the most part, is freely filtered; thus, clearance of endogenous creatinine is a reflection of ?

Back 99

is a reflection of GFR

The amount of urinary creatinine derived from tubular secretion rises proportionally in renal failure with an increase in serum creatinine. With advancing renal failure and increase in serum creatinine, the tubular secretion proportionally increases up to 40-60%.

Front 100

Urine osmolality varies widely in health, between about 60 and 1250 mOsm/kg. The failing kidney loses its capacity to concentrate urine. A patient with polyuria due to chronic renal failure (CRF) is unable to produce either a dilute or a concentrated urine.

Back 100

Urine osmolality is a measure of concentrating power of the kidney

Front 101

When evaluating SUN/creatinine ratios realize that SUN production is dependent on available protein (increased protein intake_________the ratio) and liver function (decreased liver function ___________ the ratio).

Back 101

increases

lowers

Front 102

Increased tubular reabsorption of urea occurs with decreased tubular flow as a result of dehydration, decreased cardiac output, or shock (= prerenal azotemia), or due to renal disease, such as early acute glomerulonephritis, malignant nephrosclerosis, or postrenal obstruction.

Back 102

SUN (BUN): Creatinine ratio

Front 103

Decreased ratios are seen in the presence of decreased urea synthesis (chronic glomerulonephritis with protein deficiency, severe hepatic insufficiency, and starvation) and decreased urea reabsorption (overhydration and rapid hydration).

Back 103

SUN (BUN): Creatinine ratio

Front 104

Azotemia (increase of urea or other non-protein nitrogenous - compounds) is divided into 3 categories:

Back 104

************************************
Prerenal azotemia is caused by a decrease in renal blood flow, e.g. due to decreased cardiac output
Renal azotemia results from damage to the kidney
Postrenal azotemia is due to obstruction of urine flow, e.g. by prostatic hypertrophy or tumor

Front 105

Laboratory Findings in Acute Glomerulonephritis

Back 105

Acute diffuse inflammatory changes in the glomeruli with hematuria, RBC casts, mild proteinuria, and often hypertension, edema, and azotemia.

Front 106

Serum chemistries

Elevated SUN
Elevated creatinine
Elevated uric acid
Elevated SUN/creatinine (> 20:1)
Decreased creatinine clearance
GFR decreased
Metabolic acidosis due to retention of phosphate, sulfate, amino acids, and other metabolic acids

Back 106

acute glomerulonephritis labs

Front 107

Urinalysis

Red cells in urine
Microscopic hematuria (Smoky urine)
Macroscopic hematuria (Red urine)
Casts: Red cell casts (Blood casts)
Proteinuria, mild to moderate

Back 107

acute glomerulonephritis urinalysis

Front 108

elevated alk phosphatase in chronic glomerulonephritis

Back 108

Secondary to hypocalcemia stimulating secretion of parathyroid hormone)

Front 109

the concentration of a substance dissolved in the blood above which the kidneys begin to remove it into the urine

Back 109

renal threshold

*When the renal threshold of a substance is exceeded, reabsorption of the substance by the proximal renal tubuli is incomplete; consequently, part of the substance remains in the urine.

Front 110

Indeed, the most common reason for the glucose renal threshold ever being exceeded is?

Back 110

diabetes

Front 111

The routine urinalysis is carried out in three phases:

Back 111

macroscopic (physical), chemical, and microscopic analysis.

Front 112

Macroscopic Examination (Gross Examination)

Back 112

Color
Turbidity

Front 113

Chemical Examination
of the urinalysis

Back 113

Specific gravity (Normal, 24 hours: 1.010-1.025)
Protein
Glucose
Ketone bodies
Hemoglobin (Occult blood)
Note: Myoglobin also reacts
Bile (Direct or conjugated bilirubin reacts, but not unconjugated)
Urobilinogen

Front 114

Microscopic examination of urinalysis

Back 114

Microscopic Examination

Larger elements are: casts, mucous threads, parasites, ova, foreign bodies, etc. (low power)
Casts, if present, are also examined under the high power field to determine their types
The numbers of red cells, white cells, epithelial cells, bacteria, yeast, trichomonas, and crystals are also counted and an average count for each is recorded

Front 115

urine casts

Back 115

Casts are found in the urine sediment. They are formed in two ways, by precipitation and gelling of proteins in tubular fluid, and by clumping of cells in tubules. Casts are molded in the lumen of the distal renal tubules or collecting ducts. The matrix of all casts is a specific mucoprotein common to all casts, namely Tamm-Horsfall protein.

Front 116

White blood cell (leukocyte) casts.
These casts are formed when WBC's are incorporated into the protein matrix.
example?

Back 116

pyelonephritis

Front 117

Azotemia-

Back 117

An excess of urea and/or other nitrogenous compounds in the blood

Front 118

Casts-

Back 118

Casts- Protein aggregates, outlined in the shape of renal tubules and excreted into the urine. The matrix is the
Tamm-Horsfall protein

Front 119

Creatinine clearance-

Back 119

Creatinine clearance- An estimate of the glomerular filtration rate obtained by measurement of the amount of
creatinine in the plasma and its rate of excretion into the urine

Front 120

Glomerular Filtration Rate (GFR)-

Back 120

Glomerular Filtration Rate (GFR)- The rate in milliliters per minute that substances such as creatinine and
urea are filtered freely through the kidney’s glomeruli; a reflection of the number of functioning nephrons.
Estimated by the creatinine clearance

Front 121

Nephritis accompanied by inflammation of the capillary loops in the glomeruli of the kidney; occurs in acute, subacute, and chronic forms and may be secondary to hemolytic streptococcal infection; evidence suggesting possible immune or autoimmune mechanisms

Back 121

Glomerulonephritis-

Front 122

Low-grade, dipstick-negative increase in urine albumin excretion, useful in monitoring
renal status of individuals prone to renal impairment from diseases such as diabetes.

Back 122

Microalbuminuria-

Front 123

Inflammation of the kidney with focal or diffuse proliferation or destructive processes that may
involve the glomerulus, tubule, or interstitial renal tissue.

Back 123

Nephritis-

Front 124

General name for a group of diseases involving increased glomerular permeability,
characterized by massive proteinuria and lipiduria with varying degrees of edema, hypoalbuminemia, and
hyperlipidemia.

Back 124

Nephrotic Syndrome-

Front 125

Pyelonephritis

Back 125

Pyelonephritis- Inflammation of the kidney and its pelvis

Front 126

The presence of pus (an inflammation fluid with leukocytes and dead cells) in the urine.

Back 126

Pyuria-

Front 127

A mucoprotein produced by the ascending limb of the loop of Henle that is a normal
constituent of urine and is the major protein constituent of urinary casts

Back 127

Tamm-Horsfall protein

Front 128

An excess in the blood of urea, creatinine, and other nitrogenous end products of protein and amino
acid metabolism; more correctly referred to as azotemia

Back 128

Uremia

Front 129

The two most popular screening tests for renal function are

Back 129

serum urea nitrogen (SUN/BUN) and serum creatinine

*Better measures of glomerular function are clearance tests. This is especially true in the aged, where
serum creatinine measurements are less reliable due to decreasing muscle mass.

Front 130

In uremia (kidney failure) the increase is mainly in ______, ________ and uric acid

Back 130

urea, creatinine

Front 131

In hepatic failure the ratio of non-urea/urea
nitrogen increases, because

Back 131

of the inability of the liver to synthesize urea and to deaminate amino acids

Front 132

acute phase proteins/reactants

Back 132

a class of proteins whose plasma concentrations increase (positive acute-phase proteins) or decrease (negative acute-phase proteins) in response to inflammation. This response is called the acute-phase reaction (also called acute-phase response).

Front 133

"Negative" acute-phase proteins decrease in inflammation. Examples include albumin,[4] transferrin,[4] transthyretin,[4] retinol-binding protein, antithrombin, transcortin. The decrease of such proteins may be used as markers of inflammation

Back 133

Positive acute-phase proteins serve different physiological functions for the immune system. Some act to destroy or inhibit growth of microbes, e.g., C-reactive protein, Mannose-binding protein, complement factors, ferritin, ceruloplasmin, Serum amyloid A and haptoglobin. Others give negative feedback on the inflammatory response, e.g. serpins. Alpha 2-macroglobulin and coagulation factors affect coagulation, mainly stimulating it.

Front 134

"Negative" acute-phase proteins __________in inflammation. Examples include albumin,[4] transferrin,[4] transthyretin,[4] retinol-binding protein, antithrombin, transcortin. The decrease of such proteins may be used as markers of inflammation

Back 134

decrease so can be used as indication of inflammation

albumin (trensthyretin, retinol-binding protein)
transferrin

Front 135

a protein found in the blood, the levels of which rise in response to inflammation

Back 135

C-Reactive Protein:

(i.e. C-reactive protein is an acute-phase protein)
*bind to phosphoCholine expressed on the surface of dead or dying cells (and some types of bacteria) in order to activate the complement system via the C1Q complex.[1]

Front 136

develops in a wide range of acute and chronic inflammatory conditions like bacterial, viral, or fungal infections; rheumatic and other inflammatory diseases; malignancy; and tissue injury or necrosis.

Back 136

The acute phase response

*These conditions cause release of interleukin-6 and other cytokines that trigger the synthesis of CRP and fibrinogen by the liver.

Front 137

Measuring _________ level is a screen for infectious and inflammatory diseases.

Back 137

CRP

* Rapid, marked increases in CRP occur with inflammation, infection, trauma and tissue necrosis, malignancies, and autoimmune disorders.

Front 138

CRP hits a limit within 6 hours and peaks at ___ hours.
The rate of CRP can tell the ____ of the inflammation.

Back 138

CRP rises up to 50,000-fold in acute inflammation, such as infection. It rises above normal limits within 6 hours, and peaks at 48 hours. Its half-life is constant, and therefore its level is mainly determined by the rate of production (and hence the severity of the precipitating cause).

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CRP is not present in scleroderma, etc. It IS present in?

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THINK VESSELS:

*CRP level is an independent risk factor for atherosclerotic disease. **Patients with high CRP concentrations are more likely to develop stroke, myocardial infarction, and severe peripheral vascular disease.

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In its absence, neutrophil elastase is free to break down elastin, which contributes to the elasticity of the lungs, resulting in respiratory complications such as emphysema, or COPD (chronic obstructive pulmonary disease) in adults and cirrhosis in adults or children

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alpha-1 antitrypsin

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are a group of globular proteins in plasma,[1] which are highly mobile in alkaline or electrically charged solutions. They inhibit certain blood protease and inhibitor activity

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alpha globulins

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α1-antitrypsin
Alpha 1-antichymotrypsin
Orosomucoid (acid glycoprotein)
Serum amyloid A
Alpha 1-lipoprotein

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alpha 1 globulins

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Haptoglobin
Alpha-2u globulin
α2-macroglobulin
Ceruloplasmin
Thyroxine-binding globulin
Alpha 2-antiplasmin
Protein C
Alpha 2-lipoprotein
Angiotensinogen

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alpha 2 globulins

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name the active phase reactants that indicate inflammation or liver failure

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haptoglobin
CRP
ceruplasminin (alpha 2 globulin)

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name the proteins that go down when the acute phase reactants go up, because the liver is trying to conserve amino acids

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albumin,
transferrin
transthyretin
retinol-binding protein

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antibodies are also called

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Immunoglobulins

Gamma globulin proteins used by immune system to identify and neutralized antigens like bacteria and viruses

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why measure acute phase reactants/proteins?

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Measurement of acute-phase proteins, especially C-reactive protein, is a useful marker of inflammation in both medical and veterinary clinical pathology. It correlates with the erythrocyte sedimentation rate (ESR).

They may also indicate liver failure [

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A macroglobulin is a plasma globulin of high molecular weight.

ELEVATED LEVELS of macroglobulin (macroglobulinemia) causes?

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Elevated levels of macroglobulins (macroglobulinemia) may cause manifestations of excess BLOOD VISCOSITY (as is the case for IgM antibodies in WALDENSTROM macroglobulinemia)

and/or precipitate within blood vessels when temperature drops (as in cryoglobulinaemia).

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Macroglobulin associated with NEPHROTIC SYNDROME & DIABETES

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Alpha 2 macroglobulin = nephrotic syndrome & diabetes

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abnormal bands on SPE

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Abnormal bands (spikes) are seen in monoclonal gammopathy of undetermined significance and multiple myeloma, and are useful in the diagnosis of these conditions.

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gamma globulins (general)

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Gamma globulins are a class of globulins, identified by their position after serum protein electrophoresis. The most significant gamma globulins are immunoglobulins ("Igs"), more commonly known as antibodies, although some Igs are not gamma globulins, and some gamma globulins are not Igs.

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There are 5 different classes of antibodies found in serum. They are Immunoglubulin A, M, D, E and G.

Which one is gamma globulin?

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IgG

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gamma globulin 3

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CRP
IgG (is gamma globulin)
IgM most usually hypergammaglobulinemia culprit meaning inflammation like plasmocytoma, multiple myeloma, or Waldenstrom's macroglobulinemia

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>20:1

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Pre renal: reduced blood flow, causes elevated BUN reabsorption in the kidney but Creatinine is not reabsorbed so ratio goes up!

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10-20:1

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Normal/Post-renal (within ureter) is normal range. Could be post renal back flow from obstrucition (ie stones) causing elevated BUN. Creatinine is not reabsorbed, ergo the BUN:Cr ratio increases just like in pre-renal

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<10:1

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Intrarenal dz within the kidneys
Renal damage causes reduced BUN reabsortpin and therfore lowers the BUN:Cr to closer within each other's numbers

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in Acute gouty nephropathy, you lose your

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kidney due to massive cell destruction

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In Chronic gouty nephropathy, there is

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long term inflammation due to deposition of crystals in kidney