4. Bleeding Disorders Flashcards

1
Q

Introduction
􏰓Bleeding- common in dentistry
􏰓____ patients in a dental clinic will have a form of bleeding disorder
􏰓Little to no clinical risk in most patients
􏰓____ risk group – bleeding alteration from
disease or drugs
􏰓Important to diagnose prior to initiating treatment- helps prevent fatalities

• It’s important that you expect the risk. You want to prevent fatalities from happening. Or you want to prevent ____ periods of treatment.

A

1 in 20
high
prolonged

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2
Q

Recognizing patients with bleeding disorders

􏰓History taking
􏰓____ and Surgical hx 􏰓Medication list
􏰓Personal and Family hx
􏰓____ hx

􏰓 ROS
􏰓Easy ____ or bruising 􏰓Nose bleeds
􏰓____ bleeds

• Little things like ____, NSAIDs, ____ are medications that increase the risk of bleeding. You want to know these medications***
• As you take your family history, you want to ask, “Any bleeding disorders in the family?
◦ “Any dads, uncles, grandpas with a bleeding history” when you’re thinking of Recessive X-
linked disorders.
◦ When its a female–> you want to ask “Do you have irregular or heavy bleeds during your
____ cycle?” You’re trying to rule out a bleeding disorder when you ask this.

A

medical
gyn

bleeding
gingival

aspirin
warfarin
menstrual

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3
Q

Recognizing patients with bleeding disorders

􏰓Clinical Examination – ____, ecchymoses
􏰓observation of excessive bleeding after a surgical procedure
􏰓For major invasive surgical procedures all patients should be screened for platelet ____, aPTT, ____, TT

A

petechiae
count
PT

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4
Q

Hemostasis

Primary phase
􏰓____ phase
􏰓____ phase

Secondary phase
􏰓____ phase

􏰓____ phase- where clot is dissolved

A

vascular
platelet
coagulation
fibronlytic

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5
Q
  • These are your endothelial cells of your blood vessel.
  • So now you have an injury (breach to epithelium). Blood wants to come out this way.

• Blood vessels will constrict to prevent further blood loss. ◦ That’s termed the “____ Phase of Hemostasis”
• In the blood flowing through the vessels, platelets will aggregate where you have a breach in the epithelium. In the presence of von Willebrand Factor (vWF, helps the platelets adhere together and to the wall of your blood vessel), you have the formation of a temporary Platelet Plug.
◦ This is termed the “____ Phase of Hemostasis”
• Your blood is not flowing out anymore. But this temporary plug is not stable nor solid, so it can easily be ____.

• You have clotting factors also within the blood that is flowing. They go through the Clotting Cascade (described in the next slide) and end up forming a ____ in the area where your temporary plug is. That forms a more stable clot.
◦ This is termed the “____ Phase of Hemostasis” where you have coagulation factors coming in and forming the Fibrin Mesh.

• At the end of this, after the Fibrin Mesh has been formed, the final process is to repair the vessel. Once the vessel is repaired, you don’t need the platelet plug/clotting factors anymore. The clot breaks down and that ends your hemostasis process.
◦ This is termed the “____ Phase of Hemostasis”

◦ She wants us to remember this, the fact that ____ breaks down your clot

A

vascular
platelet
dislodged

fibrin mesh
coagulation

fibrinolysis
fibrinolysis

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6
Q

• For the instrinsic pathway, you have Factor ____ that becomes activated and actives Factor ____. Becomes activated, actives Factor ____. Becomes actived, activates Factor ____.
◦ Remember, I skipped Factor 10 somehow. It didn’t get lost. It’s a member of the ____ pathway.

• For the extrinsic pathway, you have ____ that becomes activated and activates Factor ____. Becomes activated, activates Factor ____.
◦ So both instrinsic and extrinsic pathway come together when Factor 10 is activated to form the Common Pathway.

A
12
11
9
8
common

tissue factor
7
10

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7
Q
  • When Factor 10 is activated (Common Pathway) in the presence of [____, Factor 5, ____], you have ____ activated. When Thrombin is activated, it activates ____, which ends up forming your Fibrin Clot. This is only one process of forming Fibrin Clots.
  • Another process of forming Fibrin Clots is actually Factor 2 (____) which directly activates Thrombin, and this also would end up giving you the Fibrin Clots.

• So 2 processes are occuring here to get your Fibrin Clot.
◦ 1) The ____ cascade through the instrinsic & extrinsic pathway forming the Common Pathway
◦ 2) From ____ forming Thrombin which activates Fibrinogen to form Fibrin.

A

calcium
lipids
thrombin
fibrinogen

prothrombin

coagulation
prothrombin

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8
Q

• For the intrinsic pathway, the lab study we carry out to know if a disorder is coming from this pathway is
____
• For the extrinsic pathway, it’s ____ or ____ which tells you the PT based on standardized values so you don’t get different numbers in different geographic locations.
◦ INR= ____
◦ So if you have a standard or mean INR, and you take the average of your INRs from the different laboratories (around the world), and you divide by this [Standard Normal Prothrombin Time], you should
always get the same INR.
◦ So you can have different PT’s from the patient, but when you divide by the [Standard Normal
Prothrombin Time], you should always end up with the same INR number.
◦ The normal value of a patient without a bleeding problem is 1.0.

A

activated partial thromboplastin time (aPPT)
prothrombin time (PT)
INR
PT / [standard normal prothrombin time]

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9
Q
Vitamin k dependent clotting factors
􏰓Factor \_\_\_\_ 
􏰓Factor \_\_\_\_
􏰓Factor \_\_\_\_
􏰓Factor \_\_\_\_
A

II
VII
IX
X

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10
Q

What are bleeding disorders?

􏰓Conditions that affect:
􏰓 Blood vessels ____
􏰓____ production/function 􏰓____ factors

  • Bleeding disorders are disorders that could affect the Vascular Phase, Platelet Phase, Coagulation Phase, or Fibrinolytic Phase of Hemostasis.
  • When you talk about Vascular Phase disorder, it could be a problem with the ____ wall itself or a problem with the connective tissue.

• When you talk about Platelet Phase, it could be a problem with ____ of platelets. If you have a low # of platelets, you have an increased risk of bleeding. You can also have problems with the function of the platelets.
◦ Remember when I mentioned ____ Factor? I said that it helps with platelet aggregation and adherence of the platelets to the wall of the endothelium.
◦ So I might have an adequate # of platelets, but if some of the glycoproteins that help platelets adhere together are not functional or present, it can also lead to bleeding problems. The platelets are there, but they can’t do anything.
◦ You can have problems with the function or the # of platelets.

A
integrity
platelets
coagulation
vascular
number
von willebrand
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11
Q

What are bleeding disorders?

• You can also have ____ factor problems in that the coagulation factors can be deficient (have an inadequate #)

• You can have problems with coagulation inhibitors (____) which help prevent excessive clotting there.
◦ The antibodies (Protein C, Protein S) go within the bloodstream to prevent excessive clotting. But if they’re hyperactive, where you have these factor inhibitors, when they’re too abundant, you have too much ____.
◦ In sum–> Its goal is to prevent clotting. But if they’re too abundant, it leads to excessive bleeding.

• Even though the Fibrinolysis Phase is to breakdown your clots, if it’s happening too ____, it can lead to bleeding.

A

coagulation
protein C, protein S
bleeding
rapidly

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12
Q

Lab studies - bleeding disorders

Lab studies - bleeding disorders
􏰓Platelet count: ____ cellsmm3
􏰓Normal Prothrombin time (PT): ____ seconds
􏰓Partial thromboplastin time (PTT): ____ seconds
􏰓Thrombin time (TT): ____ seconds
􏰓PFA 100
􏰓Bleeding time- no ____ in use

• Complete Blood Count is always a standard to rule out a bleeding disorder.
◦ It will have red blood cell, white blood cell, platelets, and your differentials for your red blood
cells and white blood cells.
◦ The ____ are what we’re specifically looking for here (for bleeding disorders)
‣ The normal platelet count is important to know. When you know this figure, you’ll know if there’s a problem and you’ll be able to anticipate problems in your dental chair.
‣ Regular platelet count: 150,000-400,000
◦ Sometimes when you have a condition called ____, where you have too much
red blood cells, you’re also concerned with the red blood cell count.

A
150,000-400,000
11-13.5
25-35
12-14
longer

platelets
polycythemia vera

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13
Q

Lab studies - bleeding disorders

◦ Ask for normal Prothrombin Time (PT). This is for ____ pathway. [reads normal]
◦ Activated Partial Thromboplastin time (aPPT) is for ____ pathway [reads normal]
◦ Thrombin Time (TT) tells you from when ____ is activated to when Fibrin is formed.
Sometimes they will request TT.
◦ In the past, they used Bleeding Time, but that didn’t tell you much about the function of your
platelets. No longer in use.
◦ These days, they use more of the ____.
◦ In addition to your CBC, they also do a ____ Smear. This tells you about the morphology
of your platelets. Are they too big or too small?

A
extrinsic
intrinsic
factor 10
platelet function analyzer 100
peripheral
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14
Q

Concerns with Platelet count
􏰓____ cells/mm3 – mild bleeding after trauma
􏰓____ cells/mm3– moderate bleeding after trauma
􏰓

A

50,000-100,000
20,000-50,000
20,000
2

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15
Q

Bleeding disorders
􏰓 ____
􏰓 ____/congenital

A

acquired

inherited

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16
Q
Acquired bleeding disorder
􏰓 \_\_\_\_
􏰓 Drugs
􏰓 \_\_\_\_
􏰓 Chemotherapy

• Medications: patients with bleeding disorders are on these, some have to do with clotting factors ◦ There are a lot of anti-platelet medications
‣ Plavix: being used in patients with ____ or patients at risk of ____
◦ Sometimes anti-____ medications
• Radiation usually would lead to ____ of the precursors that will form platelets in the bone marrow.
◦ Patients that receive radiation therapy are at risk for ____. This could lead to an aquired bleeding disorder because of deficient platelets.

• Same thing in ____. It’s killing the cancer cells in patients with Leukemia and things like that. ◦ In killing the cancer cells, the precursor cells are sometimes targeted and that also leads to
deficiency in platelets (thrombocytopenia).

A

disease
radiation

atrial fibrillation
DVT
coagulation
depletion
chemotherapy
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17
Q

Acquired bleeding disorder
􏰓Disorders affecting ____ phase
􏰓Disorders affecting ____ phase
􏰓Disorders affecting ____ phase

A

vascular
platelet
coagulation

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18
Q

Acquired bleeding disorders
􏰓Vascular defects:
􏰔____ vessel malformation
􏰔Acquired ____ tissue (CT) disorders

A

structural

connective

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19
Q

Vascular defects- acquired CT disorders

􏰓Small vessel vasculitis
􏰓Any conditions that cause ____ of small vessels- arterioles, venules and capillaries

􏰓Arteriovenous Malformation 􏰓____ most common
􏰓____ > Female
􏰓

A

inflammation
brain AVM
male
1

arteriovenous malformation (AVM)
uterine
brain
blood vessels

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20
Q

Acquired vascular defects - acquired CT disorders

  • SCURVY

____ def > weakened ____ fibers > defective ____ supportive tissue > capillary ____

• Scurvy is an acquired CT disorder. It leads to fragility of your blood vessel wall because your CT is not intact. Scurvy can weaken your ____ and lead to capillary fragility.

A
vit. C
collagen
perivascular
fragility
collagen fibrils
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21
Q

Acquired vascular defects - acquired CT disorders

  • STEROID USE (long term)

thinning of ____ tissue > bleeding after ____ trauma

• If a patient is also on long-term steroid use, if they just bump their hands, they bleed. Their CT becomes thinner the longer they’re on steroids. So they have a high risk of bleeding after minor trauma.

A

connective

minor

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22
Q

Vascular defects- acquired CT disorders

  • SERUM SICKNESS

____ deposits into vessel walls > ____ (skin hemorrhage - 4-10mm)

􏰓Serum-sickness like reactions:
􏰓drug-induced- ____, hydralazine, ____, diuretics 􏰓____ induced

  • Serum sickness is a kind of reaction to horse serum which is used in the treatment of things like ____ and Diptheria. It’s an ____ reaction to horse serum causing fever, rashes, and arthralgia. It makes the CT of the blood vessel more fragile and can lead to bleeding under the skin (purpura).
  • Even though horse serum is what causes Serum Sickness, some medications give a similiar presentation of the arthritis, rashes and fever. They are termed Serum-sickness like reactions. Some of these medications include ____ (??)(which is an antibiotic), penicillins, ____ and diuretics.
A
immune complex
purpura
penicillin
sulphonamide
hepatitis

scarlet fever
allergic
cephalaco
sulfonamides

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23
Q

Acquired platelet disorder - Platelet function disorder

􏰓Platelets- form ____ for the adherence of clotting factors
􏰓Involved in clotting cascade by release of platelet ____
􏰔Serve as constituents of ____
􏰔Serve as constituents of ____ converting complexes

  • The platelets and coagulation factors really interact in forming your temporary clot. The platelets also interact in the presence of platelet ____ to help stabilize your Fibrin Mesh.
  • You could have problems with the platelet number. or function of the platelets.
A
scaffold
factor 3
factor X
prothrombin
factor 3
24
Q

Acquired Platelet function disorder (PFD)

􏰓Drugs- ____, β- lactam antibiotics, ____ channel blockers, Aspirin
􏰓Diseases- ____ dx, liver failure, ____
􏰓Foods/supplements- ____, garlic, ____, omega-3 fatty acids

• Ca channel blockers: things like Nifedipine, Verapamil can impair the normal functioning of your
platelets

• Certain food supplements like ____ fatty acids or garlic and ginger. You might have heard that if you’re on Warfarin you have to avoid garlic and ginger. In patients, garlic and ginger also cause impairment of platelets (they are natural ____, basically).
◦ So in patients that already have a bleeding problem, this can impair their platelet function further

A
NSAIDS
Ca
kidney
tumeric
omega-3
blood thinners
25
Q

Acquired coagulation disorder- DIC

Clinical presentation:

􏰓Acute DIC
􏰔Accelerated ____
􏰔Bleeding from small wounds 􏰔____
􏰔Spontaneous bleeding

􏰓Chronic DIC: e.g. ____, SLE 􏰔____ (blood clots are formed)

• DIC: disseminated intravascular coagulopathy
◦ Can occur after ____ (usually viral), surgery or after snake bites
◦ It can go 2 ways. In the acute form, you’re having too much breakdown of your ____ that is
formed. Normally, ____ helps you break down clots at the end of hemostasis. But this is happening too rapidly and this causes bleeding or hemorrhage.
◦ When you have it in the chronic form, it results in ____ clotting.
◦ DIC is when you’re concerned about ____. You can see bleeding under the skin (purpura).

A

fibrinolysis
purpura

cancers
thrombosis

fibrin
fibronolysis
excessive
bleeding

26
Q

Management of DIC

􏰓____ ( if bleeding)
􏰓 FFP
􏰓____ ( if thrombosis)
􏰓Platelet replacement, clotting factor replacement
􏰓Avoid use of plasmin and plasmin product inhibitors e.g. ____

  • If a patient has acute DIC, you want to give them Cryoprecipitate. It’s a product of plasma that contains ____ and ____ factors. The patient is bleeding, so you want to ensure that you’re having clot formation. You can also give them ____.
  • If a patient has chronic DIC, you want to give ____. It’s an anti-thrombin inhibitor. It works on thrombin to make sure you’re having less clotting occuring.
A

cryoprecipitate
heparin
tranexamic acid

fibrinogen
clotting
fresh frozen plasma (FFP)

heparin

27
Q

ACQUIRED Fibrinolytic disorder

  • Hyperfibrinolysis
  • Too much ____
    – early breakdown of clots
  • ____ disease
  • severe trauma
  • PT, aPTT or TT – not ____ in diagnosis
  • For your acquired fibrinolytic disorders, you have too much fibrinolysis or too rapid breakdown of your clots which will lead to bleeding also.
  • If your plasminogen is in excess, it causes too much ____ of clots. You can also see this associated with severe trauma or patients with liver disease.
  • With fibrinolysis, its the dissolution of the clot. Even though the patient is bleeding, the PT, aPTT, or TT do NOT play a role in diagnosis of hyperfibrinolytic problems.
A

plasminogen
liver
helpful
breakdown

28
Q

Acquired bleeding disorders -Liver disease
Most coagulation factors are produced in the ____.
Liver disease if significant can cause severe bleeding
Also risk of ____ from platelet sequestration in spleen
Heavy ____ -causes liver damage

• Since the spleen sequesters the platelets, so if it is hyper-functioning the platelets will be broken down and lead to more of a bleeding risk

A

liver
thrombocytopenia
alcoholism

29
Q

Other conditions -acquired bleeding disorders

  Chronic leukemia –\_\_\_\_ phase disorder
  Vit.K Malabsorption syndrome/ long term \_\_\_\_ therapy (intestinal bacteria producing Vit K maybe affected)
  End stage renal disease   \_\_\_\_
  Infections -?\_\_\_\_ 
–Hemorrhagic fevers
A

platelet
antibiotic
hypersplenism
viral

30
Q

Indirect thrombin inhibitors - Heparin

Inhibits ____ and thrombin
Given by ____ infusions
Need to monitor ____
Half life is ____hours(standard heparin)
LMWH- ↑ activity on Factor ____ e.g. enoxaparin (lovenox)
v ____ half-life (2-4hrs) vSubcute. ____

• LMWH - low molecular weight heparin
◦ Remember this: regular heparin is given through IV and LMWH is subcutaneous*
◦ LMWH is preferred because…
‣ It has double the half life of normal heparin
‣ You don’t have to monitor your aPTT as regularly as you would with normal heparin

A
factor Xa
IV
aPTT
1-2
Xa
longer
administration
31
Q

Direct thrombin inhibitor
Dabigatran (Pradaxa) Orally administered
Used to prevent ____ in patients with
____

A

stroke

a. fib

32
Q

Factor Xa inhibitor
____ (Xarelto)
Apixaban (Eliquis)
Both ____ administered

A

rivaroxaban

orally

33
Q

Vit. K dependent coagulation protein inhibitor

Warfarin (Coumarin)

____
competitively inhibits ____ (enzyme for Vit K activation)
Inhibits factors ____, VII,____,X ____ administered
Monitored with ____

A
anticoagulant
vitamin K epoxide reductase complex 1
prothrombin (II)
IX
orally
PT/INR
34
Q

Inherited bleeding disorders

Not as common as ____ bleeding disorders
Epidemiology: 10-20 in 2000 patients

A

acquired

35
Q

Congenital/inherited bleeding disorders
Alteration of vascular wall
Hereditary hemorrhagic telangiectasia

  • bleeding defect > problem w wall ____ > ____
  • most ____ defect
A

integrity
petechiae
common

36
Q

Congenital/Inherited – Platelet disorder
____ dx
Bernard- Soulier
Glanzmann thrombasthenia

____ syndrome
____ anomaly
____
- these three > abnormal platelets larger in size and fewer in number

A

von willebrand
gray platelet
may-hegglin
hereditary thrombocytopenia

37
Q

Congenital/inherited bleeding disorders
Disorders of coagulation
Hemophilia A ( factor ____ def) Hemophilia B(factor ____ def)

Primary congenital deficiencies of fibrinolytic inhibitors
____ [A2AP]
____ [PAI-1]

A

VIII
IX
alpha-2-antiplasmin
plasminogen activator inhibitor-1

38
Q

Vascular defect- Hereditary hemorrhagic telangiectasia

  \_\_\_\_
  1:8000to 1:50000 Petechiae
\_\_\_\_ have inherent mechanical fragility
  Noted on \_\_\_\_ membranes   Tx: \_\_\_\_, surgery, \_\_\_\_
replacement, thalidomide
A
rare
blood vessels
skin and mucous
laser
hormonal
39
Q
Congenital connective tissue disorders associated with bleeding
\_\_\_\_ disease
  Osteogenesis imperfect
  \_\_\_\_ elasticum
  Marfan syndrome
A

ehlers-danlos

pseudoxanthoma

40
Q

Von Willebrand disease- platelet function disorder

  Most \_\_\_\_ inherited bleeding disorder
  Affects 1% of US population
\_\_\_\_ trait –mild to moderate clinical bleeding
 type 1 (70-80%cases)
  type 2A(15-20%cases)
\_\_\_\_ form (Type 3)   Other forms- rare
A

common
autosomal dominant
autosomal recessive

41
Q

Von Willebrand disease– signs and symptoms
Mild forms-____/cutaneous bleeding
Severe forms: ____, dissecting intramuscular ____

A

mucosal
hemarthrosis
hematoma

42
Q
Diagnosis of Von Willibrand’s dx
  Prolonged \_\_\_\_ (\_\_\_\_ is normal) 
  \_\_\_\_ or low platelet count
von Willebrand specific: 
   \_\_\_\_ cofactor activity - – vWF to GP 1b
  \_\_\_\_ induced platelet aggregation. 
vWF \_\_\_\_
  Specific factor \_\_\_\_ assay
A
aPTT
PT
normal
ristocetin
ristocetin
immunoassay
VIII
43
Q

Treatment
Desmopressin-risk of thrombosis in ____ patients with ____
____ acid
____ (prepared from plasma)- contains ____, factor VIII, ____ fibrinogen, factor XIII

Factor ____ replacement that retainsvWF

A

elderkly
CVD

aminocaproic
cryoprecipitate
vWF
fibronectin

VIII

44
Q

Bernard- Soulier disease
Caused by lack of ____ which prevents binding of vWF to platelets
platelets ____ and defective
Clinical features- skin ____, epistaxis,
irregular heavy menstrual bleeding
Tx: platelet ____, desmopressin, Factor ____

A
glycoprotein Ib
large
bleeding
transfusion
VIIa
45
Q

Glanzmann thrombasthenia

Disorder of platelet aggregation
Abnormality of platelet membrane complex ____ (fibrinogen receptor)
____ trait
Platelets adhere to ____ (via
vWF) but cannot bind to ____
Higher frequency with consanguinity e.g.
____, Iranians etc

A
glycoprotein IIb/IIIa
autosomal recessive
subendothelium
fibrinogen
indians
46
Q

Gray platelet syndrome

Very ____
Abnormal platelet disorder – ____ and ____ # of platelet
____ gene disrupt the normal production of alpha-granules
____ - fibrous scar in bone marrow

A
rare
large
decreased
NBEAL2
myelofibrosis
47
Q

Coagulation disorder-
Hemophilia A

  Factor \_\_\_\_ deficiency
  Most \_\_\_\_ inherited coagulation
bleeding disorder
  1 in every 5000 male births   
\_\_\_\_ trait
  Clinical manifestation- \_\_\_\_, hematoma, \_\_\_\_
A
VIII
common
x-linked recessive
ecchymosis
hemarthrosis
48
Q

Hemophilia A

Lab findings, prolonged ____, normal PT and ____ count.
Management: avoid ____,

A

aPTT
platelet
NSAIDS

49
Q

Coagulation disorder-
Hemophilia B

Deficient factor ____
____ trait

A

IX

X-linked recessive

50
Q

Oral manifestations of bleeding disorders

  \_\_\_\_ in oral mucosa
  Spontaneous gingival bleeding
  \_\_\_\_
  Jaundice
  \_\_\_\_
  TMJ Hemathrosis –\_\_\_\_ factor disorder
A

petechiae
ecchymosis
pallor
coagulation

51
Q

Oral manifestations of bleeding disorders

Enlarged ____ glands- ____ liver dx (usually alcoholism)
Leukemia-generalized gingival ____ & bleeding
Neoplasm-osseous lesions, ____, oral ulcers, loosening of teeth, ____ (burning,numbnessinlip)

A
parotid
chronic
enlargement
tumors
paresthesia
52
Q

Signsand symptomsof bleeding disorders
Vascular phase- ____ and ____ membrane/skin bleeding

Platelet phase – ____, ____

Coagulation phase- ____,
hemathrosis, ____,

A

petechiae
mucous

petechiae
ecchymosis

ecchymosis
hematoma

53
Q

Platelet disorder
Bleeding after cuts and sutures: ____
Bleeding post surgery/trauma: ____

Coagulation disorder
Bleeding after cuts and sutures: ____
Bleeding post surgery/trauma: ____

A

yes
immediate

no
delayed

54
Q

Dental management

Thrombocytopenia -

A

30,000

80,000 to 100,000

55
Q

Dental mangt (contd)

____ dental care important in hemophiliacs
Avoid ____ block, IM injections, injection into ____, lingual infiltration
____ (5%),orally or before and after extraction

A

preventive
IAN
FOM
tranxemic acid

56
Q

Dental management (contd)
Avoid ____ in patients taking warfarin
INR should be between ____ in at risk pt groups (taking warfarin)
Avoid ____, broad spectrum antibiotics in this group of pts
Follow up within ____ hrs after surgical procedures

A

aspirin
2-3.5
NSAIDS
24-48