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Clin Path Midterm Q7 > Clinpath Midterm > Flashcards

Clinpath Midterm Flashcards

1
Q

For the test what is the normal color of urine?

A

Blue.

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2
Q

What are the 2 ways in which we have the inability to regulate hemostasis?

A
  1. Hemorrhage. 2. Thrombosis.
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3
Q

What type of state is thrombosis?

A

Hypercoagulable state.

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4
Q

What are the 2 categories of bleeding disorders?

A
  1. Coagulation associated bleeding. 2. Platelet associated bleeding.
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5
Q

What are the 2 types of coagulation associated bleeding?

A

Inherited and acquired.

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6
Q

How can you tell if a bleeding condition is congenital?

A

most of the major congenital bleeding disorders are coagulation- associated disorders. Congenital disorders tend to manifest earlier in life.

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7
Q

How should a new vs old bleeding disorder be treated?

A

New- immediate diagnostic and treatment preferably by a specialist. Old- careful monitoring but no further diagnostic testing.

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8
Q

Coagulation-associated bleeding is usually bleeding where?

A

Into joints.

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9
Q

What is bleeding in joints called? What can repeated joint bleeding cause?

A

Hemarthrosis. Can cause degeneration as an arthritic change.

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10
Q

Platelet-associated bleeding is usually what?

A

Mucous membrane, or mucocutaneous bleeding or brusing.

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11
Q

Name different types of brusing?

A

Petechiae, ecchymosis, purpura.

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12
Q

Genetic bleeding disorders tend to be what type of inheritance?

A

Sex-linked.

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13
Q

How can drugs/ medications cause bleeding disorders?

A

Asprin causes platelet function to be altered. Some drugs can supress bone marrow production of platelets. Platelet function or production may be affected via idiosyncratic drug reactions.

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14
Q

Name systemic diseases that might cause bleeding disorders?

A

Recent infections, presence of other hematologic diseases, nutritional deficiencies, autoimmune diseases, liver diseases.

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15
Q

What are signs and symptoms of other hematologic disorders?

A

Anemia, lymphadenopathy, splenomegaly, bone pain.

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16
Q

Name the 3 congenital coagulation-associated bleeding disorders?

A

Hemophilia A, Hemophilia B, Von Willebrand’s disease.

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17
Q

What causes Hemophilia A and B?

A

A- factor VIII:C deficiency. B- factor IX deficency aka christmas factor.

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18
Q

What is the most severe of the 3 congenital coagulation-associated bleeding disorders?

A

Hemophilia A.

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19
Q

What is the most common of the 3 congenital coagulation-associated bleeding disorders?

A

von Willebrand’s disease is the most common inherited hemostatic disorder.

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20
Q

Of the 3 congenital coagulation-associated bleeding diseases will they effect males or females more?

A

Hemophilia A and B more males. vWD- males equal females.

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21
Q

Where will bleeding most commonly occur at with hemophilia A?

A

Anywhere, but most commonly into large weight bearing joints and soft tissues.

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22
Q

What are the types of hemophilia A?

A

Severe, moderate, mild and they depend on the amount of factor VIII:C that is missing.

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23
Q

How common are the 3 types of hemophilia A and what are they like?

A

Severe (<1%)- evident early in life, spontaneous bleeding for no apparent reason. Moderate (1-5%)- not appatent until child attempts to place weight on large joints. Mild (5-30%)- not noticed until after trauma or surgery.

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24
Q

What is a PT test?

A

Prothrombin test- testing the extrinsic clotting pathway.

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25
Q

What is a APTT test?

A

Activated partial thromoplastin time- testing the intrinsic clotting pathway. AKA PTT.

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26
Q

What is a BT test?

A

Bleeding time- assess platelet function.

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27
Q

What is a platelet count test?

A

Just a count of total platelets done with a BT test (before you can know if the platelets are functioning normaly you need to know if you have a normal amount).

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28
Q

What are the lab findings for hemophilia A?

A

Normal- PT, Platelet count, and BT. Prolonged PTT.

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29
Q

With hemophilia A and B will they be caused by factor deficiencies or abnormal functioning factors?

A

A- deficiency and rarely dur to abnormal function. B- 2/3 is deficiency and 1/3 is abnormal function.

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30
Q

What will the lab findings be for hemophilia B?

A

Normal- PT, Platelet count, and BT. Prolonged PTT. Same as hemophilia A and they are genetically similar.

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31
Q

vWD is what type of abnormality? Caused by what?

A

Coagulation and platelet function due to dyfunctional or deficient von willebrand’s factor.

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32
Q

What is the purpose of von Willebrands factor?

A

mediates platelet adhesion and preserves VIII:C from degradation.

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33
Q

The greater majority of vWD patients only manifest what?

A

Platelet-associated bleeding.

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34
Q

How many types of vWD are there and which one is most common?

A

5 subtypes and type I makes up 80%.

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35
Q

What is type I vWD like?

A

clinically mild quantitative deficiency in vWF.

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36
Q

The most common vWD patient will display what type of bleeding?

A

Mild provoked bleeding following trauma, surgery, and dental extractions. Some women can have abnormal menstral bleeding.

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37
Q

A type I vWD patient may become more evident when?

A

With the use of asprin since the asprin will further decrease the platelet’s ability to adhere.

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38
Q

What are the lab results for a vWD patient?

A

Normal- PT, Platelet count, PTT (rarely prolonged only when VIII:C is <25% of normal and this will not happen with subtype I). Prolonged- BT(occasionally normal, but can be provoked with an asprin challenge).

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39
Q

What are 2 types of aquired coagulation-associated bleeding disorders/

A

Hepatic insufficiency. Vitamin K deficiency.

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40
Q

What will happen with hepatic insufficiency (Hemostasis related)?

A

Leads to bleeding tendency due to decreased production of coagulation proteins.

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41
Q

What coagulation factors need Vitamin K?

A

II, VII, IX, X.

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42
Q

What can lead to vitamin K deficiencies?

A

Biliary tract disease due to malabsoprtion due to fat absorption problems. Nutritional deficit is rare. Broad-spectrum antibiotics destroy GI flora that normally produce Vitamin K.

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43
Q

Besides coagulation factors what coagulation proteins are important?

A

Some that inhibit fibrinolysis (continued consumption of coagulation factors).

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44
Q

What causes fibrinolysis (or a loss in the factors that inhibit fibrinolysis)?

A

This is a late effect of a severly compromised liver.

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45
Q

How else will a cirrhotic liver effect hemostasis?

A

Reduction in thrombopoietin and this leads to thrombocytopenia.

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46
Q

What are the lab findings with early and late hepatic insufficiency?

A

Early- Normal- APTT, platelet count, BT, prolonged PT. Late- Prolonged PT, APTT, BT, Decreased Platelet count. Vitamin K antagonisitc medication like Warfarin.

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47
Q

What would lab tests be like for a pateint with mild vitamin K deficiency or on theraputic doses of Warfarin?

A

Both would have normal APTT, Platelet count and bleeding time and Prolonged PT.

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48
Q

What is INR?

A

International normalized ratio for patients on Coumadin or Warfarin. PT values are used to monitor patients on oral anticoagulants like coumadin and warfarin.

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49
Q

What are the 2 things that can cause thrombocytopenia?

A

Bone marrow not making enough platelets or something happens to them once in circulation.

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50
Q

Thrombocytopenia is what type of bleeding disorder?

A

quantitative (not enough) platelet-associated bleeding disorder.

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51
Q

Name the things that can cause thrombocytopenia due to bone marrow suppression?

A

aplastic anemia (lost ability to produce blood cells), leukemias (normal bone marrow is being replaced with malignant and remaining bone marrow cant keep up), metastatic lymphoma or carcinoma replacing bone marrow, folic acid or B12 deficiencies, chemotherapy and radiation therapy, viral infections (HBV, EBV, HIV, CMV), Drugs (including alcohol).

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52
Q

What is the name of a disease that causes thromobyctopenia due to peripheral platelet destruction?

A

Idiopathic thrombocytopenia purpura (ITP).

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53
Q

What causes ITP?

A

Autoimmune phenomenon where IgG mediated antibodies coat platelets resulting in splenic sequestering of platelets.

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54
Q

What type of bleeding will ITP cause?

A

Mucocutaneous bleeding, epistaxis, bleeding gums, prupura, petechiae, menorrhagia.

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55
Q

Will ITP cause splenomegaly?

A

no.

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56
Q

What are the 2 types of ITP?

A

Acute and chronic.

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57
Q

When will acute and chronic ITP begin? What will the onset be like?

A

Acute- pediatric and abruptly. Chronic- adult with insiduous onset.

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58
Q

What will cause acute and chronic ITP?

A

Acute- 80% post viral infection. Chronic- associated with other systemic dieases such as malignancy, other autoimmune diseases, rarely with viral infections.

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59
Q

What is acute and chronic ITP like and How long will acute and chronic ITP last?

A

Acute- short course markedly reduced platelet count (<20K) then it will spontaneously go into remission. Chronic- longer clinical course up to years with platelet count 20-100K and will rarely spontaneously go into remission.

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60
Q

How can acute and chronic ITP be treated?

A

Acute- supportive. Chornic- corticosteroids or splenectomy.

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61
Q

What is anemia?

A

The hematologic state in which the number of RBC, the amount of hemoglobin, and the volume of RBC is less than normal resulting in a pathologic deficiency in oxygen-carrying capacity of blood.

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62
Q

When should anemia be suspected?

A

Mucous membrane pallor (best place to see is conjunctiva since pallor due to anemia is not always pale complection), fatigue, generalized weakness, dizziness, headaches, tinnitus (ringing or buzzing in ears), palpitations, tissue changes in lips or tounge, peripheral neuropathy.

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63
Q

What general populations have higher prevalence of anemia?

A

Pregant, elderly over 75 years, nutritionally unbalanced diets.

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64
Q

In general what are the reference ranges like for hemoglobin?

A

Smaller in children and highest in adult males and slightly lower levels in pregnant females vs adult females.

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65
Q

What are the 2 general ways of classifying anemia?

A

RBC indicies. Pathophysiology.

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66
Q

What are the 3 types of anemia based upon RBC indicies?

A
  1. Microcytic hypochromic. 2. Normocytic normochromic. 3. Macrocytic.
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67
Q

What are the types of microcytic hypochormic anemias?

A

iron deficiency, thalassemias (faultly synthesis of hemoglobin), chronic diseases

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68
Q

What are the types of normocytic normochromic anemias?

A

hypoplastic bone marrow, chronic diseases, hemolytic anemias.

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69
Q

What are the types of macrocytic anemias?

A

B12 and folate deficiencies.

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70
Q

What are the 3 types of anemias based upon pathophysiology?

A

factor deficiency, production defect, hemolytic.

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71
Q

What are the factor deficiency anemais?

A

Iron, B12 and folate deficiencies.

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72
Q

What are the production defect anemias?

A

Chronic disease, hypoplastic bone marrow.

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73
Q

What 5 things lead to an increased risk of iron deficiency anemia (IDA)?

A
  1. Deficient diet. 2. Decreased absorption. 3. increased requirments like growth spurts. 4. Pregnancy. 5. Blood loss.
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74
Q

What causes IDA in all adults until proven otherwise?

A

Bleeding.

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75
Q

What 2 types of bleeding often lead to IDA in adults?

A

Gynecological and GI.

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76
Q

When will signs of IDA be seen?

A

Late in deficiency due to insiduous nature of onset.

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77
Q

What is peripheral blood like with early decreases in iron storage?

A

Normal.

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78
Q

What will peripheral blood be like with depleted storages of iron?

A

Early changes will be increased RDW. Decreased RBC, HgB, Hct, and MCV MCH and MCHC decreased.

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79
Q

What will serum iron panel be like with an IDA patient that has not had treatment?

A

Decreased; serum iron, % saturation, serum feritin. Increased- TIBC.

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80
Q

What type of anemia is iron deficiency?

A

Microcytic and hypochromic.

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81
Q

What will peripheral blood be like once the depleted storage of iron problem has been fixed, but not replenished?

A

RBC, HgB, HcT increase. Temperature increases. RDW increases. Indicies increase.

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82
Q

What is thalassemia?

A

Anemia caused by faulty synthesis of hemoglobin.

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83
Q

What will serum iron panel be like with an IDA patient that has started treatment?

A

Decreased; TIBC. Increased; Serum iron, % saturation, serum ferritin.

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84
Q

Which iron panel will be the best indication of iron storage?

A

Serum ferritin and it takes the longest time to return to normal.

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85
Q

What would a typical CBC look like for an IDA patient?

A

Low HGB and HCT= anemia. Low MCV= microcytic. Low MCH and MCHC= hypochromic.

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86
Q

When you get a CBC that looks like IDA what should be done?

A

Check for bleeding problems and Order Serum iron studies before iron supplementation starts.

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87
Q

Why should you order serum iron studies first?

A

It could be from loss of blood not just diet issues.

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88
Q

What would a CBC look like for a Vitamin B12 and Folic acid anemias?

A

Low HGB and HCT= anemia. High MCV= macrocytic. Normal MCH and MCHC= normochromic.

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89
Q

What are the 2 general types of macrocytic anemias and what causes them?

A
  1. Megaloblastic anemai= B12 and Folate. 2. Non-megaloblastic= ethanol, liver disease, hypothyroidism.
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90
Q

From a CBC how can you distinguish a B12 from a folate deficiency?

A

You cant they look identicle.

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91
Q

What is B12 used for?

A

It is needed for the proper utilization of Folic Acid in the synthesis of DNA and therefore both are needed for appropriate cellualr growth.

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92
Q

B12 and folate deficiencies result in what?

A

Ineffective erythropoiesis and marcrocytic cells that will lead to intramedullary hemolysis due to increased size.

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93
Q

B12 and folate deficiencies lead to asynchronous maturation of blood cells which leads to what?

A

Neutropenia, hypersegmentation of the neutrophils and mild thrombocytopenia (not to the level of spontaneous bleeding).

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94
Q

What are the signs and symptoms of B12 and folate deficiences besides the normal anemic ones?

A

Neuropsyciatric and GI signs and symptoms.

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95
Q

Where and how is vitamin B12 absorbed?

A

Must be bound to intrinsic factor and is absorbed in the terminal ileum.

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96
Q

Where will intrinsic factor come from?

A

Gastric parietal cells.

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97
Q

What is Vitamin B12 and folate acid storage like?

A

B12- stored in liver and can hold 2-3 years worth of B12. Folate- stored in liver but only 2-4 months worth.

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98
Q

What are the causes of B12 deficiency?

A
  1. Diet. 2. Malabsorption. 3. Drugs.
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99
Q

What is the major dietary source of B12?

A

Meats and dairy.

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100
Q

What are the types of malabsorption that leads to B12 deficiency?

A
  1. No intrinsic factor. 2. Gastrectomy. 3. Blind loop syndrome. 4. tape worm. 5. Ileum diseases.
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101
Q

What is pernicious anemia?

A

An autoimmune condition that will cause gastric mucosa loss and lead to a decrease in intrinsic factor.

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102
Q

How will a gastrectomy cause B12 deficency?

A

Loss of stomach musoca and cant produce intrinsic factor.

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103
Q

What is blind loop syndrome and how will it affect B12 absorption?

A

Outpouching of gut and bacteria of gut overgrows the loop and the bacteria here can consume B12.

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104
Q

How will fish tapeworm lead to B12 deficency?

A

Eats B12.

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105
Q

name a disease of the ileum that affects B12 absorption and why?

A

Crohn’s disease- if it affects the terminal illeum it can lead to a decrease in B12 absorption.

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106
Q

What drugs will cause a B12 deficiency and how?

A

Alcohol- can lead to gastritis and damage the lingin and interefer with intrinsic factor production. Nitrous oxide- prolonged use can damage bone marrow and nervous system by interfering with the ACTION of B12.

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107
Q

What would routine serum chemistry tests show for a B12 or folic acid anemia?

A

Unconjugated hyperbilirubinemia and increased LDH. Both of these will come as a result of RBC lysis since they are macrocytic.

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108
Q

What tests can be done if you suspect B12 deficiency?

A

Serum Vitamin B12. Serum methylmalonic acid (MMA).

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109
Q

A patient with B12 deficiency will have what results from a serum B12 and a MMA test?

A

Serum B12- decreased and MMA- increased.

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110
Q

What is the relationship with MMA and B12?

A

Without B12 MMA levels go up and this may be seen before serum B12 levels go down.

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111
Q

If you know a patient has a B12 deficiency what tests can be done to determine if it is pernicious anemia?

A

Schiling test if positive is due to lack of intrinsic factor but is not specific for pernicious anemia so you can run a anti-intrinsic factor and anti-gastric parietal cell antibody tests.

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112
Q

What will anti-intrinsic factor and anti-gastric parietal cell antibody tests screen for?

A

both for pernicious anemia. Anti-intrinsic factor is (60% specific for pernicious anemia) and anti-gastric parietal cell antibodies are (90% specific for PA).

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113
Q

What are the clinical features that are common to both B12 and Folate deficiencies?

A

Megaloblastic anemia, macrocytic, fatigue, weight loss, diarrhea, loss of appetite, fever, sore tounge, jaundice, fundal hemorrhages in severe cases.

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114
Q

What are the clinical features that are common to just B12 deficiency?

A

Parestheisa, dementia, neuropathy, demyelination of spinal cord.

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115
Q

Wha tare the clinical features specific to pernicious anemia?

A

family or personal history of vitiligo, autoimmune thyroid disease.

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116
Q

What would jaundice skin look like due to anemia?

A

Lemon-yellow due to pallor and jaundice.

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117
Q

Name 4 things that can cause a Folic acid deficiency?

A
  1. Dietary insufficiency. 2. Malabsorption. 3. Drugs. 4. Increased requirements.
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118
Q

What types of foods have folic acid?

A

Fresh fruits, vegetables and grains. (not over cooked).

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119
Q

What other type of diet besides inadequate consumption can cause folic acid deficiency?

A

Alcohol- The primary metaboite for alcohol degrades folate in the colon. Folate acid deficiency is a common sign of alcoholism. Alcohol also inhibts absorption of folate.

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120
Q

What type of things cause malabsoprtion of folate?

A

Celiac’s disease and Alcohol.

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121
Q

How will drugs cause folic acid deficiencies?

A

Folic acid is a sticky molecule and drugs stick to it and render folic acid inert.

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122
Q

What type of people have an increased requirement for folic acid?

A

pregnancy, infancy, malignancy, exfoliative skin diseases.

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123
Q

What will lab findings be like for folic acid deficiencies?

A

CBC, routine serum chemistry same as B12.

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124
Q

IF you have an anemia and suspect a folic acid deficiency what special chemistry tests should you do?

A

Serum folate- which would be decreased. Serum homocysteine- which should be increased.

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125
Q

What would a CBC look like for a patient that has anemia due to a chronic illness?

A
  1. 80 % of the time it will be Low HgB, HcT= anemia. Normal MCV= normocytic. Normal MCH,, MCHC= normochromic. 2. 20% of the time due to blocked release of iron by macrophages during transfer and will cause decreased HgB, HcT= anemia. Decreased MCV= microcytic. and decreased MCH, MCHC= hypochromic.
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126
Q

Name 6 chronic diseases that commonly produce anemia?

A

renal, liver, rheumatologic (inflammatory), infectious, malignant, endocrinologic.

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127
Q

What is pancytopenia?

A

a condition of hypoplastic bone marrow that suppresses erythropoietic activity or replaces active healthy marrow with fibrotic or malignant tissue and occurs to the entire myeloid hematopoietic activity. The marrow activity can be totally suppressed in some cases and this is called aplastic anemia.

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128
Q

What are 2 general causes of depletion (hemolytic)anemias?

A
  1. Extracorpuscular agent induced (aquired). 2. Intracorpuscular defect induced (inherited).
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129
Q

What is extracorpuscular agent induced?

A

good bone marrow but you have things like; immunohemolytic, traumatic, toxin, parastic.

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130
Q

What is intracorpuscular defect induced?

A

Bone marrow produces bad RBC that will be destroyed.

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131
Q

What are the 3 types of bad RBC produced due to intracorpuscular defects?

A
  1. hemoglobin abnormalities like thalassemia (faulty hemoglobin), or hemoglobin S disorders. 2. RBC membrane abnormalities- hereditary spherocytosis. 3. RBC enzyme abnormalites- G-6-PD deficiency.
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132
Q

What would the results be of a CBC for a patient with a hemolysis anemai?

A

Low HgB, HcT= anemia. Reticulocytosis (increase of immature RBC showing bone marrow is active and trying to make up for anemia).

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133
Q

What would the results be for a serum test on a patient with hemolysis anemia?

A

Since RBC are lysing you would have unconjugated hyperbilirubinemia and increased LDH (since RBC are full of LDH and heme- which is converted into unconjugated bilirubin once outside the RBC). In extreme cases the plasma can turn pink due to free hemoglobin.

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134
Q

What would the urine tests show with a hemolytic anemia?

A

Hemoglobinuria- presence of hemoglobin in urine not RBC. Hematuria- would not be seen with hemolytic anemias and this is the presence of RBC in urine.

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135
Q

What would be seen on x-ray of a hemolytic anemic patient?

A

Erythroid hyperplasia causing thinning of the bone.

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136
Q

What is immunohemolytic anemias that cause extracorpuscular agent induced hemolytic anemais?

A

Intravascular or intrasplenic hemolysis of RBC due to either isoantibodies or autoantibodies.

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137
Q

Name a disease that is immunohemolytic anemia?

A

Hemolytic disease of the newborn (HDN).

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138
Q

How will traumatic events cause extacorpuscular induced anemias?

A

Physical trauma to RBC causes hemolysis.

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139
Q

What are things that can cause traumatic hemolytic anemias?

A

May occur in malignant hypertension, surgical replaced heart valves, reptetive external blows to the body.

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140
Q

Name 3 things that can cause toxic hemolytic anemias?

A

Chemicals, burns, snake venoms.

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141
Q

How will parasites cause hemolytic anemais?

A

The plasmodium parasite (malaria) causes hemolysis during its lifestyle.

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142
Q

How can you diagnose malaria?

A

During pateints high fever take a blood sample and do a smear and look for parasites.

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143
Q

What type of anemia will thalassemias be?

A

Microcytic hypochromic.

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144
Q

What are the 3 things that can lead to thalassemias?

A

Hypoproilferative anemia, hemolytic anemia, and abnormal hemoglobin synthesis.

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145
Q

What are the 2 types of thalassemias and how can you tell them apart on a CBC?

A

Alpha- no increased RBC. Beta- increased RBC starting with the minor beta thalassemias.

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146
Q

What type of people are more likely to have a thalassemia?

A

Alpha- SE Asians, Chinese, and blacks. Beta- mediterraneans, Chinese, other Asians and blacks.

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147
Q

Genetically what causes Alpha and Beta thalassemias?

A

Alpha- you inherit one, two, three, or four gene deletions that reduce the synthesis of alpha chains. Beta- point mutations of genes may produce a homozygous or heterozygous reduction of beta chains.

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148
Q

What will the Hemoglobin electrophosesis look like for Beta thalasemias?

A

Decreased HbA1 and increased HbA2 and HbF.

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149
Q

What will cause a minor vs more serious alpha thalassemia?

A

Minor will one- two gene deletions three is more serious. Four gene deletions will result in a stillborn fetus.

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150
Q

What is the homozygous form of beta thalassemias like?

A

Homozygous- excess alpha chains are unstable and percipitate leading to damaged RBC membranes which leads to intramedullary and intravascular hemolysis with increased hemolysis and ineffective EPO the bone marrow becomes hyperplastic and expands leading to bony deformities.

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151
Q

What are the different manifestations of beta thalassemia?

A

Minima, minor, intermedia and major.

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152
Q

Which beta thalassemias will be anemic?

A

Minor, intermedia and major with Increased RBC.

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153
Q

What will a CBC look like for Alpha thalassemias?

A

Decreased MCV and MCH with Target cells.

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154
Q

What will a CBC look like for beta thalassemias?

A

Decreased MCV and MCH with target cells and stippling.

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155
Q

How can you tell an Iron deficiency from a thalassemia from a CBC?

A

Both will have decreased MCV but Iron anemias will rearely lower the MCV below 70 and Thalassemias will often lower the MCV below 70.

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156
Q

Is hemoglobin S abnormalities a thalassemia?

A

No.

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157
Q

Genetically what causes hemoglobin S abnormalities?

A

Point mutations that substitute valine for glutamine in the 6th position of the beta chain.

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158
Q

What will hemoglobin S abnormalities do to hemoglobin?

A

HbS forms polymers that damage the RBC membrane and cause sickling.

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159
Q

Sickling of RBC is primarily influenced by what?

A

The amount of HbS present and hypoxemia.

160
Q

Early damage to RBC from HbS can do what?

A

it can be reversible, but multiple episodes causes irreversible sickling.

161
Q

What are the 2 types of hemoglobin S abnormalities?

A

Sickle cell trait. Sickle Cell anemia.

162
Q

What is the genetic difference between Sickle cell trait and sickle cell anemia?

A

Sickle cell trait- heterozygous. Sickle cell anemia- Homozygous.

163
Q

Who will be more likely to get sickle cell trait and by how much?

A

American blacks and 8% will have it.

164
Q

What will sickle cell trait be like?

A

usually no hemolytic episodes or complications, but in rare instances sickling crisis can occur when patient is involved in vigorous exercies and exposed to an extremely hypoxic environment. They may have renal tubular function abnormalities resulting in dilute urine and hematuria (unexplained).

165
Q

What tests can be done on someone suspected of sickle cell trait?

A

(+) dithinoite solubility test for HgB S, and HgB electrophoresis will show some HgB S at about 35-45%.

166
Q

What % of American blacks will have sickle cell anemia?

A

0.15% will.

167
Q

What will sickle cell anemia be like?

A

Failure to thrive becomes apparent within 6 months after birth. Vasoclusive phenomena results in multiple system involvment; skeleton, viscera, skin and eyes.

168
Q

What are the lab findings like for sickle cell anemia?

A

Marked anemia, circulating sickle cells, circulating nucleated RBC’s (immature), leukocytosis (due to tissue necrosis), thrombocytosis, 80% HgB S from electrophoresis.

169
Q

What are 3 things that can happen to sickled RBC?

A

Lysis, clumping and clogging small blood vessels, accumulate in spleen.

170
Q

What will a CBC for a sickle cell anemia patient look like?

A

Really low RBC, Low HgB and HcT. Low leukocytes and will show target cells and sickle cells.

171
Q

What will Hereditary spherocytosis cause?

A

RBC membrane abnormality and is rare.

172
Q

What will a glucose-6-phosphate dehyrogenase (G6PD) deficiency cause?

A

A lack in NADPH which is needed to resist oxidative stress and hemoglobin becomes unstable causing lysis.

173
Q

What can cause the oxidative stress?

A

Acute infections, foods (like fava bean), drugs, etc.

174
Q

What is another name for G6PD deficiency?

A

favism and this comes from fava beans which have a chemical that can cause G6PD deficiency.

175
Q

What is are the disorders that primarily manifest in neoplastic proliferation of a bone marrow cell line?

A

Leukemias and myeloproliferative disorders.

176
Q

What will usually make the leukocyte count go up or stay the same with leukemias?

A

If malignant cells are in peripheral blood then count will go up or be normal. If the malignant cell is not in the peripheral circulation you could have leukopenia.

177
Q

If leukemians and myeloproliferative disorders are gone untreate what will happen?

A

They will succum to infection secondary to severe granulocytopenia or bleeding secondary to lack of platelets.

178
Q

What will life span be like for people with acute leukemia?

A

it is measured in days or weeks.

179
Q

What will the life span be like for people with chronic leukemias?

A

one to two years.

180
Q

What is the onset of acute leukemias like?

A

short period from time of first symptom until they seek care.

181
Q

What are the 2 types of acute leukemias?

A

Acute lymphoblastic leukemia (ALL), acute myelogenous leukemia (AML).

182
Q

What is the difference between ALL and AML?

A

AML- primarily an adult disease. ALL- primarily a kids disease between ages 2-10.

183
Q

What is bleeding like for acute leukemias?

A

usually in the skin and mucosal surfaces.

184
Q

What will infections be like for acute leukemias?

A

due to neutropenia and have the risk of infection becoming high as the neutrophil count falls belwo 500.

185
Q

What other problems (besides bleeding and infections) are seen with acute leukemias?

A

Gum hypertrophy, bone and joint pain.

186
Q

What areas will commonly have bone pain with acute leukemias?

A

sternum and tibia.

187
Q

What happens in severe cases of acute leukemias?

A

Impaired circulation resulting in headache, confusion, and dyspena.

188
Q

What will a physical exam be like for someone with acute leukemia?

A

pallor, purpura, petechiae, various signs of infection, gum hypertrophy, hepatomegaly, splenomegaly, and lymphadenopathy.

189
Q

What will lab findings be for acute leukemia?

A

pancytopenia (an abnormal reduction in the number of red blood cells, white blood cells, and blood platelets in the blood), circulating blasts.
pancytopenia (an abnormal reduction in the number of red blood cells, white blood cells, and blood platelets in the blood), circulating blasts.
pancytopenia (an abnormal reduction in the number of red blood cells, white blood cells, and blood platelets in the blood), circulating blasts.
pancytopenia (an abnormal reduction in the number of red blood cells, white blood cells, and blood platelets in the blood), circulating blasts.
pancytopenia (an abnormal reduction in the number of red blood cells, white blood cells, and blood platelets in the blood), circulating blasts.
pancytopenia (an abnormal reduction in the number of red blood cells, white blood cells, and blood platelets in the blood), circulating blasts.
pancytopenia (an abnormal reduction in the number of red blood cells, white blood cells, and blood platelets in the blood), circulating blasts.
pancytopenia (an abnormal reduction in the number of red blood cells, white blood cells, and blood platelets in the blood), circulating blasts.
pancytopenia (an abnormal reduction in the number of red blood cells, white blood cells, and blood platelets in the blood), circulating blasts.
pancytopenia (an abnormal reduction in the number of red blood cells, white blood cells, and blood platelets in the blood), circulating blasts.
pancytopenia (an abnormal reduction in the number of red blood cells, white blood cells, and blood platelets in the blood), circulating blasts.
pancytopenia (an abnormal reduction in the number of red blood cells, white blood cells, and blood platelets in the blood), circulating blasts.
pancytopenia (an abnormal reduction in the number of red blood cells, white blood cells, and blood platelets in the blood), circulating blasts.
pancytopenia (an abnormal reduction in the number of red blood cells, white blood cells, and blood platelets in the blood), circulating blasts.

190
Q

What type of blasts will be circulating for ALL and AML?

A

ALL- lymphocytic. AML- myelocytic.

191
Q

What will cause panctopenia with acute leukemias?

A

bone marrow is being replaced by other tissues so normal bone marrow volume goes down.

192
Q

What will a CBC look like for acute leukemia?

A

Hard to say. Probably will be anemic. Probably increased WBC, but may be normal or increased (important to check differential). Platelets will probably be normal.

193
Q

Name the 4 types of myeloproliferative disorders?

A
  1. polycythemia vera (PV). 2. Chronic myelogenous leukemia (CML). 3. Myelofibrosis (with myeloid metaplasia). 4. Essential thrombocythemia (ET).
194
Q

What are myeloproliferative disorders?

A

Chronic leukemias.

195
Q

Who is more likely to get a myeloproliferative disorder aka chronic leukemias?

A

People over 50 and males>females.

196
Q

What are the signs and symptoms of polycythemia vera?

A

symptoms related to expanded blood volume and increased viscosity like; headache, dizziness, tinnitus, blurred vision, fatigue, prunitus and epistaxis. Renal veins are engorged, ruddy cyanotic skin, hepatosplenomegaly, gout and thrombotic events.

197
Q

What are the lab findings with Polycythemia vera?

A

Panmyelosis (Myeloid metaplasia with abnormal immature blood cells in the spleen and liver) erythrocytosis, granulocytic leukocytosis, thrombocytosis.

198
Q

What will the thrombocyte count be like with polycythemia vera?

A

As high as 2000 when reference is (150-450).

199
Q

What are the signs and symptoms of CML?

A

fatigue, malaise, weight loss, night sweats, low-grade fever, abdominal fullness (splenomegaly), sternal tenderness (marrow over expansion).

200
Q

What are the lab findings like for CML?

A

Elevated WBC count with a distinct shift to the left, basophilia, possible anemias, variable platelet counts, philidelphia chromosome detectable.

201
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.

202
Q

What is the philidelphia chromosome responsible for?

A

95%- CML. 5%- down syndrome.

203
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.

204
Q

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

A

abdominal fullness, fatigue (due to anemia).

205
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.

206
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.

207
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.

208
Q

Name 2 types of chronic lymphoproliferative leukemic disorders?

A
  1. Chronic lymphocytic leukemia (CLL). 2. Hairy cell leukemia (HCL).
209
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.

210
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).

211
Q

When will CLL be detected usually?

A

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

212
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.

213
Q

Who is more likely to get hairy cell leukemias?

A

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

214
Q

What are the signs of HCL?

A

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

215
Q

What are lab findings like for HCL?

A

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

216
Q

What are plasma cell dyscrasias?

A

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

217
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).
218
Q

What are the signs and symptoms of multiple myeloma like?

A

Low back pain is the most common initial symptom.

219
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.

220
Q

Multiple myeloma is the most common malignat disease of what?

A

Plasma cells.

221
Q

Who is most likely to get multiple myeloma?

A

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

222
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).

223
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.

224
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).

225
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.

226
Q

What will hypervisocity syndrome lead to?

A

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

227
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.

228
Q

What are the serology lab tests like for multiple myeloma?

A

Markedly elevated ESR due to hypergammaglobulinemia.

229
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.

230
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.

231
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.

232
Q

How is a bence-jones protein detected?

A

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

233
Q

How common are bence-jones proteins with multiple myeloma?

A

75% of patients with MM will have them.

234
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.

235
Q

What type of protein is bence-jones?

A

M-paraprotein.

236
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.

237
Q

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

A

Bone marrow aspiration.

238
Q

What is waldenstrom macroglobulinemia?

A

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

239
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.

240
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.

241
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.

242
Q

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

A

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

243
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.

244
Q

How are lymphomas diagnosed?

A

Via lymph node biopsy.

245
Q

Name the 2 types of lymphomas?

A

Hodgkin disease, and nonhodgkins lymphoma

246
Q

What is hodgkin’s disease like?

A

Malignant lymph node with reed-sternbery cells.

247
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.

248
Q

What are the lab findings for hodgkins disease?

A

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

249
Q

What is nonhodgkins lymphoma?

A

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

250
Q

What are the clinical findings seen with nonhodgkins lymphoma?

A

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

251
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.

252
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.

253
Q

What level of hematuria warrants investigation?

A

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

254
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.

255
Q

Hematuria may be the only and first sign of what?

A

Early urinary tract pathology.

256
Q

What are the 2 categories of hematuria?

A

Without casts or without proteinuria, with casts and proteinuria.

257
Q

What are the types of hematuria without casts or proteinuria?

A

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

258
Q

What are the types of hematuria with casts and proteinuria?

A

acute glomerulonephritis, chronic glomerulonephritis, rheumatoid disease.

259
Q

Proteinuria may be the first and only sign of what?

A

Early urinary tract pathology.

260
Q

Name 4 reasons for developing proteinuria?

A
  1. Functional proteinuria (minimal amounts). 2. Overload proteinuria (pre-renal). 3. Glomerular proteinuria. 4. Tubular proteinuria.
261
Q

Name 4 tests used to evaluate kidney function?

A
  1. Clearance test. 2. Creatinine clearance. 3. Serum blood urea nutrogen. 4. Serum creatinine.
262
Q

What will the clearance test screen for?

A

Mild to moderate diffuse glomerular damage.

263
Q

What is creatinine?

A

The end product of skeletal muscle metabolism.

264
Q

What will levels of creatinine in serum represent?

A

skeletal muscle mass not activity.

265
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.

266
Q

The serum creatinine levels have the same significance as what?

A

Renal azotemia.

267
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.

268
Q

Increased BUN equals what?

A

Azotemia.

269
Q

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

A

only 50%.

270
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).
271
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.

272
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.

273
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

274
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.

275
Q

Oligouria can result in what?

A

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

276
Q

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

A

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

277
Q

What happens after someone gets strep throat?

A

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

278
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.

279
Q

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

A

Hematuria, RBC casts, proteinuria, azotemia.

280
Q

What is Chronic renal failure (CRF)?

A

Progressive and irreversible destruction of nephrons regardless of the cause.

281
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.

282
Q

Why will CRF patients be anemic?

A

Kidney cant make enough EPO.

283
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.

284
Q

What are the 3 stages of CRF?

A
  1. Diminished renal reserve- measurable loss of renal function. 2. renal insufficiency- azotemia. 3. Uremia.
285
Q

What is uremia?

A

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

286
Q

What are the toxic effects seen from protein metabolites?

A

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

287
Q

Broadcasts are usually only seen with what condition?

A

Chronic kidney failure.

288
Q

Increased specific gravity means what?

A

lost the concentrating ability of the kidney.

289
Q

What should you think of when you hear nephrotic syndrome?

A

Proteinuria.

290
Q

What is nephrotic syndrome?

A

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

291
Q

Name some diseases that cause damage to the glomerular structures?

A

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

292
Q

Nephrotic syndrome is aka?

A

secondary nephrotic syndrom since it is caused by systemic diseases.

293
Q

What type of things are seen with nephrotic syndrome?

A

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

294
Q

What is idiopathic nephrotic syndrome?

A

A type of nephrotic syndrome with an unknown cause.

295
Q

When will an idiopathic nephrotic syndrome be diagnosed?

A

At childhood.

296
Q

How is an idiopathic nephrotic syndrome diagnosed?

A

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

297
Q

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

A

Normal.

298
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.

299
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.
300
Q

What is sterile pyuria?

A

WBC in urine with negative bacteriologic evaluation.

301
Q

What can cause strile pyuria?

A

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

302
Q

What is pyelonephritis?

A

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

303
Q

What are the 2 types of pyelonephritis?

A

Acute and chronic.

304
Q

What is the clinical presentation of acute pyleonephritis like?

A

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

305
Q

What will the onset of acute pyleonephritis be like?

A

Acute onset.

306
Q

What is seen in urine with acute pyelonephritis?

A

Marked pyuria, WBC clumps, WBC casts and proteinuria.

307
Q

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

A

Clumps- bladder infections. Casts- kidney infections.

308
Q

What is a chronic pyelonephritis like?

A

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

309
Q

What is cystitis?

A

An inflammed bladder usually caused by an infected bladder.

310
Q

Who will be more likely to get a bladder infection?

A

Women.

311
Q

What are the presentations of cystitis?

A

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

312
Q

What are the routine findings on urinalysis for a cystitis?

A

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

313
Q

What tests on a urinalysis will show up with bacteriuria?

A

Leukocyte esterase and nitrite.

314
Q

What is a normal history of a women with cystitis?

A

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

315
Q

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

A

vaginal irritation and or discharge.

316
Q

What are the 3 types of prostatitis?

A
  1. Acute bacterial prostatitis. 2. chronic bacterial prostatitis. 3. Nonbacterial prostatitis.
317
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.

318
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.

319
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.
320
Q

What is more common acute or chronic bacterial prostatitis?

A

Chronic.

321
Q

What causes chronic bacterial prostatitis?

A

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

322
Q

What is the history like for chronic bacterial prostatitis?

A

Usually no history of previous acute bacterial prostatitis.

323
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.

324
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.

325
Q

What are some possible causes of nonbaceterial prostatitis?

A

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

326
Q

What is more common chronic bacterial or nonbacterial prostatitis?

A

Nonbacterial prostatitis.

327
Q

What are the findings with nonbacterial prostatitis?

A

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

328
Q

What is urethritis and what are the 2 types?

A

Inflammation of the urethra. Gonococcal and nongonococcal.

329
Q

Gonococcal urethritis commonly effects who?

A

Males.

330
Q

What are the clinical sings and symptoms of gonococcal urethritis?

A

penial discharge, dysuria, urethral itching.

331
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.

332
Q

What is the difference between gonococcal and nongonococcal urethritis?

A

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

333
Q

What is another name for hypertension that damages the kidneys?

A

nephrosclerosis.

334
Q

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

A

serious and irreversible renal damage.

335
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.

336
Q

Hypertension can cause a type of what?

A

chronic renal failure.

337
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).

338
Q

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

A

Azotemia.

339
Q

What is nephrolithiasis?

A

Urinary stone disease or kidney stones.

340
Q

Nephrolithiasis is the ____ most common urinary tract problem.

A

Third.

341
Q

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

A
  1. infections. 2. prostatic disorders.
342
Q

What are the main type of kidney stones?

A

Those made of calcium salts.

343
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.

344
Q

Incidnec of nephrolithiasis increased with who?

A

Sedentary lifestyle, summer months and humidity.

345
Q

What factors promote stone formation?

A

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

346
Q

What factors will inhibit stone formation?

A

citrate, increased water intake.

347
Q

What is the most common symptoms with nephrolithiasis?

A

Pain.

348
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.

349
Q

What will the patients response to the pain be?

A

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

350
Q

What are the laboratory findings for nephrolithiasis?

A

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

351
Q

What are the 2 types of urinary tract obstructions?

A

congenital and aquired.

352
Q

What are the 3 areas of urinary tract obstructions?

A
  1. Ureter. 2. bladder outlet. 3. urethra.
353
Q

What are the acquired causes of bladder outlet obstructions?

A

bladder cancer, benign prostatic hyperplasia, prostate cancer.

354
Q

What is the mean age of a diagnosed bladder cancer?

A

65 years.

355
Q

What is the male:female ratio for bladder cancer?

A

3:1 male-to-female.

356
Q

What are the known risk factors for bladder cancer?

A

Smoking, industrial dyes and solvent exposure.

357
Q

What are the clinical findings of bladder cancer?

A

ranges from none to irritative voiding.

358
Q

What are the lab findings seen with bladder cancer?

A

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

359
Q

What type of imaging should be done for bladder cancer?

A

intravenous urography, ultrasound, CT or MRI, cystourethroscopy.

360
Q

Who is most likely to get benign prostaitic hyperplasia?

A

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

361
Q

What causes benign prostatic hyperplasia?

A

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

362
Q

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

A

Obstructive and irritative.

363
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.

364
Q

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

A

Urgency, frequency, nocturia.

365
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.

366
Q

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

A

Prosate cancer (not benign prostatic hyperplasia).

367
Q

How common is prostate cancer?

A

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

368
Q

Where is prostate cancer most common at?

A

North America and Europe. Lowest is in Far East.

369
Q

What are the risk factors for prostate cancer?

A

Family history, blacks, fatty diets.

370
Q

How are prostatic cancers detected currently?

A

Digital rectal examinations (DRE).

371
Q

What are the findings seen with DRE for prostatic cancer?

A

Focal nodules, areas of indurations.

372
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.

373
Q

What is the most accurate way to detect prostatic cancer?

A

Biopsy.

374
Q

How accurate is TRUS?

A

lacks specificity and leads to too many biopsies.

375
Q

What is PSA?

A

a glycoprotein produced in the cytoplasm of prostate cells.

376
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.

377
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).

378
Q

What is a PSA density?

A

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

379
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.

380
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.

381
Q

What are the different types of PSA?

A

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

382
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.

383
Q

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

A

below 2-2.5.

384
Q

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

A

Abover 10.

385
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%).

386
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.

387
Q

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

A

Kidney tumor until proven otherwise.

388
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.

389
Q

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

A

males 2x as common as females.

390
Q

What is a risk factor for renal cell carcinoma?

A

Cigarette somking.

391
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.

392
Q

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

A

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

393
Q

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

A

fever, night sweats, weight loss, malaise.

394
Q

When will most renal cell carcinomas be detected?

A

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

395
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).

Clin Path Midterm Q7 (1 decks)

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