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189 Cards in this Set

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FEV1 less than 40% of predicted = ????

FEV1 greater 80% of predicted= normal



FEV1 60% to 79% of predicted = Mild obstruction



FEV1 40% to 59% of predicted = Moderate obstruction



FEV1 less than 40% of predicted = Severe obstruction

FEV1 40% to 59% of predicted = ???

FEV1 greater 80% of predicted= normal



FEV1 60% to 79% of predicted = Mild obstruction



FEV1 40% to 59% of predicted = Moderate obstruction



FEV1 less than 40% of predicted = Severe obstruction

FEV1 greater 80% of predicted=???

FEV1 greater 80% of predicted= normal



FEV1 60% to 79% of predicted = Mild obstruction



FEV1 40% to 59% of predicted = Moderate obstruction



FEV1 less than 40% of predicted = Severe obstruction

FEV1 60% to 79% of predicted = ?????

FEV1 greater 80% of predicted= normal



FEV1 60% to 79% of predicted = Mild obstruction



FEV1 40% to 59% of predicted = Moderate obstruction



FEV1 less than 40% of predicted = Severe obstruction

acute reversible airway obstruction... smooth muscle hyper responsiveness

asthma

asthma classification --> mild intermittent

- Day: symptoms a twice week or less


- Brief symptoms (from a few hours to a few days)


- Night: symptoms twice a month or less


- No symptoms and normal lung function between asthma "attacks”


- Spirometry results are > 80% of normal

asthma classification --> mild persistent

- Day: symptoms more than twice a week


- Night: symptoms are more than twice a month


- Symptoms may affect activity and limit exercise tolerance


- Spirometry results are > 80% of normal

asthma classification --> moderate persistent

- Day: symptoms occur every day


- Daily use of short acting inhaler


- Night: symptoms are more than once a week


- Worsening symptoms that affect activity and limit exercise tolerance


- Spirometry results are between 60% and 80% of normal

asthma classification --> severe persistent

- Day: symptoms are continual every day


- Night: symptoms are frequent > 4 times/month


- Spirometry results are 60% or less of normal

levels of asthma control - controlled

levels of asthma control - partly controlled

levels of asthma control - uncontrolled

which abx do you avoid with asthmatic patients?

Avoid clarithromycin and erythromycin and azole antifungals with theophylline



--> Azithromycin okay

which abx are good for asthmatics?

Avoid clarithromycin and erythromycin and azole antifungals with theophylline



--> Azithromycin okay

what is the analgesic of choice for asthamtics

Avoid use of aspirin and NSAIDS in sensitive patients



-–> Acetaminophen analgesic of choice for those patients

how to manage acute asthma attack

- Administer short acting β2 agonists


- Establish and maintain a patent airway


- Administer oxygen 6-10 liters via face mask, nasal hood or cannula.



If symptoms worsen


--–> Administer epinephrine subcutaneously (1:1,000 solution, 0.01 milligram/ kilogram of body weight to a maximum dose of 0.3 mg).

if acute asthma attack worsens....

- Administer short acting β2 agonists


- Establish and maintain a patent airway


- Administer oxygen 6-10 liters via face mask, nasal hood or cannula.



If symptoms worsen


--–> Administer epinephrine subcutaneously (1:1,000 solution, 0.01 milligram/ kilogram of body weight to a maximum dose of 0.3 mg).

Oral Health Changes in Individuals with Asthma

Prolonged use of β2 agonists inhalers and anticholenergics


- Increased rate of caries development


- Children with asthma have the highest caries risk


- Sugar containing medications



Reduced salivary flow due to inhaler use,


- Dry mouth associated with albuterol use.


Increased levels of gingivitis or gum disease.

inhaled corticosteroids

increased risk of candidiasis from steroids in aerosols

General Oral Health Care Instructions for asthmatics

Prescribe fluoride supplements for all asthmatic patient on β2 agonists/ anticholenergics



Instruct patients to rinse their mouths after using a steroid inhaler


–Prevention of fungal infections


–Monitor and treat as needed



Reinforce oral hygiene instructions to help minimize gingivitis

Chronic obstructive pulmonary disease (COPD)

Slowly progressive disease



Gradual irreversible loss of lung function



Includes


-Chronic obstructive bronchitis


-Emphysema,


-Combinations of both


All have three main symptoms


-Coughing


-Breathlessness


-Wheezing

mucus and inflammation

bronchitis

loss of elasticity + collapsed airways

emphysema

Clinical Features of COPD Patient


Mild COPD
-“Smokers” cough
-Little or no breathlessness



Moderate COPD
-Breathlessness with/without wheezing
-Cough with/without sputum



Severe COPD
-Breathlessness on any exertion/at rest
-Lung hyperinflation common
-Wheezing and cough prominent


-Cyanosis, peripheral edema, and polycythemia in advanced disease

pink puffer`

emphysema


--> CO2 retention,... no cyanosis... pursed lip breathing


- increased mucus, barrel chest


- no real inspiratory symptoms... but expiratory wheeze

blue bloater

bronchitis



- color cyanotic


- recurrent cough + sputum


- hypoxia.. hypercapnia


- use of accessory muscles to breathe


- overweight... heavy smokers.. lot of infections



INSPIRATORY AND EXPIRATORY SYMPTOMS


bronchitis vs emphysema

bronchitis

emphysema

which analagesics would you avoid for asthmatics?

Avoid use of aspirin and NSAIDS in sensitive patients



-–> Acetaminophen analgesic of choice for those patients

Conditions that Increase Risk of Transmission to TB Disease


• Diabetes mellitus
• End-­‐stage renal disease
• Prolonged steroid therapy
• Other immunosuppressive therapy
• Malnourishment
• HIV infection
– Strongest risk factor *****
– ~ 10% each

strongest risk factor for progression to TB disease

• Diabetes mellitus
• End-­‐stage renal disease
• Prolonged steroid therapy
• Other immunosuppressive therapy
• Malnourishment
• HIV infection
– Strongest risk factor *****
– ~ 10% each

most common way of testing for TB

mantoux skin test


--> does NOT distinguish between LTBI and TBD

Reading the Tuberculin Skin Test

Read reaction 48-72 hours after injection



Measure only induration



Record reaction in millimeters

whats a positive PPD test?

positive PPD test for someone with HIV

positive PPD test for someone with no risk factors

positive PPD test for low income drug user

how do u confirm TB dx?

use a culture

who is infectious for TB?

active symptoms of TB --> coughing



sputum positive for AFB & :


- not receiving therapy


- on therapy for < 3 weeks


- poor clinical response to therapy (still have systemic symptoms)

medical management for active TB disease

4 drugs for 4 months in initial regimen


- Isoniazid (INH)


- Rifampin (RIH)


- Pyrazinamide (PZA)


- Ethambutol (EMB) or Streptomycin (SM)



2 Drugs for 4-18 months


- Isoniazid


- Rifampin

medical management for active TB - 1st 4 drugs

4 drugs for 4 months in initial regimen


- Isoniazid (INH)


- Rifampin (RIH)


- Pyrazinamide (PZA)


- Ethambutol (EMB) or Streptomycin (SM)



2 Drugs for 4-18 months


- Isoniazid


- Rifampin

medical management for active TB - final 2 drugs

4 drugs for 4 months in initial regimen


- Isoniazid (INH)


- Rifampin (RIH)


- Pyrazinamide (PZA)


- Ethambutol (EMB) or Streptomycin (SM)



2 Drugs for 4-18 months


- Isoniazid


- Rifampin

how is infecticity for TB checked

checked with 3 consecutive negative sputums

preventative therapy for latent TB infection

- ALL pts with positive PPD should be treated !!!!!!


- prevent conversion to active disease with Isoniazid (INH)


----> 6 months for +PPD


----> 9 months for +PPD and +CXR (may add rifampin)


----> 12 months for HIV+ and +PPD


----> 18 months for HIV+ +PPD and +CXR

adverse rxns to isoniazid (inh)

- patients can't drink alcohol


- hepatotoxic (check LFTs monthly)


- 20% develop hepatititis even without alcohol


---> nausea, vomitting, abdominal pain, dark urine


- peripheral neuropathy (INH given with vit B6 to prevent this)

are surgical masks protective against TB ?

NO !!!


--> special N95 or N99 fitted respirators required

systemic signs suspicious of TB disease

- persistent productive cough (>3 weeks)


- hemoptysis


- weight loss or loss of appetite


- fever


- night sweats


- chest pain

+PPD / +CXR pt maangement

verify:


- no symptoms of active disease


- INH for 6 months - 1 year


- history of follow-up negative chest x-ray



treat as normal pt

+PPD / -CXR pt maangement

verify:


- no symptoms of active disease



Ask about history of prophylaxis


- INH for 6 months - 1 year



treat as normal pt

patients taking isoniazid (INH) for Tb... must avoid what

acetaminophen !!!!!

pts taking streptomycin must avoid what ?

aspirin !!!!

what is the main cause of chronic liver disease?

hep c

what hemostatic defects will occur in liver disease?

- Reduced clotting factors
– All but VIII

• Inhibition of coagulation
• Abnormal fibrinogen/clotting proteins

• Enhanced fibrinoly/c activity
– DIC

• Quantitative AND qualitative platelet problems

infectious hepatitis

infectious hepatitis


- viral hepatitis


- mono


- secondary syphilis


- TB



non-infectious (chemical) hepatitis


- excessive or prolonged use of toxic substances


---> drugs (acetaminophen, ketoconazole, alcohol)

noninfectious hepatitis

infectious hepatitis


- viral hepatitis


- mono


- secondary syphilis


- TB



non-infectious (chemical) hepatitis


- excessive or prolonged use of toxic substances


---> drugs (acetaminophen, ketoconazole, alcohol)

infectivity of hep-c

cal live outside body for up to 16 hours... and in a syringe for up to 63 days



high viral laods of ~800,000 .. (HIV is ~5,000)

HBsAg

Hep B surface antigen



presence indicates current Hep b infection (either acute or chronic carrier state)


presence indicates current Hep b infection (either acute or chronic carrier state)

HBsAg

Hep b anti-Hbs

presence indicates immunity to Hep B infection (ONLY if Hep surface antigen is negative)



positive if received Hep B vaccine

IgM vs IgG

Igm --> acute... recent



IgG --> disease control / immunity

HBeAg

presence indicates HIGHLY INFECTIVE stage of Hep B

presence indicates HIGHLY INFECTIVE stage of Hep B

HBeAg

Anti-HCV

presence indicates current or past hep c infection



does NOT differentiate between the acute/chronic/resolved infection

HCV-RNA

hep c RNA polymerase chain rxn



--> presence indicates actively replicating hep c virus

IgM anti HBc

IgM anti HBc --> acute infection



IgG anti-Hbc --> immunity

IgG anti-Hbc

IgM anti HBc --> acute infection



IgG anti-Hbc --> immunity

clinical significance of hep c viral load

- confirms active infection


- predictor of treatment response


- confirm HCV medications are working


- dictate treatment duration for some HCV medications



***Does not correlate with disease progression
***Does not give any info about degree of liver damage
***Has no direct impact on dental tx

does the hep c iral load correlate with disease progression

- confirms active infection


- predictor of treatment response


- confirm HCV medications are working


- dictate treatment duration for some HCV medications



***Does not correlate with disease progression
***Does not give any info about degree of liver damage
***Has no direct impact on dental tx

does hep c viral load give info about dental tx?

- confirms active infection


- predictor of treatment response


- confirm HCV medications are working


- dictate treatment duration for some HCV medications



***Does not correlate with disease progression
***Does not give any info about degree of liver damage
***Has no direct impact on dental tx

does hep c viral load give info about degree of liver damage?

- confirms active infection


- predictor of treatment response


- confirm HCV medications are working


- dictate treatment duration for some HCV medications



***Does not correlate with disease progression
***Does not give any info about degree of liver damage
***Has no direct impact on dental tx

HCV Tx

- iterferon + Ribavirin (+/- Protease Inhibitor) for 24-48 weeks



- 2 pegylated interferons FDA-improved


- pegasys


- PEG-intron



4 ribavirins


( copegus, rebetol, ribasphere, generic ribavirin)



2 protease inhibitors


- boceprevir (victrelis)


- telaprevir (incivek)

4 ribavirins

- iterferon + Ribavirin (+/- Protease Inhibitor) for 24-48 weeks



- 2 pegylated interferons FDA-improved


- pegasys


- PEG-intron



4 ribavirins


( copegus, rebetol, ribasphere, generic ribavirin)



2 protease inhibitors


- boceprevir (victrelis)


- telaprevir (incivek)

2 pegylated interferons

- iterferon + Ribavirin (+/- Protease Inhibitor) for 24-48 weeks



- 2 pegylated interferons FDA-improved


- pegasys


- PEG-intron



4 ribavirins


( copegus, rebetol, ribasphere, generic ribavirin)



2 protease inhibitors


- boceprevir (victrelis)


- telaprevir (incivek)

hematologic side effects of hep c combination therapy

- anemia


--> fatigue


--> risk of MI and other cardiovascular abnormalities



neutropenia


--> risk of infection



thrombocytopenia


--> risk of bleeding

Non-Alcoholic Related Fatty Liver Disease

- obesity, diabetes, dyslipidemia, metabolic syndrome



medications


--> amiodarone, tamoxifen, costicosteoids, HAART, tetracycline, calcium channel blockers



- malaise, fatigue, achy , abdonimaal tenderness, enlarged liver



- elevated liver enzymes, bilirubin, cholesterol, triglycerides



- CAN progress to cirrhosis and end stage liver disease !!!! ****

can NARFLD progress to cirohhsis ?

- obesity, diabetes, dyslipidemia, metabolic syndrome



medications


--> amiodarone, tamoxifen, costicosteoids, HAART, tetracycline, calcium channel blockers



- malaise, fatigue, achy , abdonimaal tenderness, enlarged liver



- elevated liver enzymes, bilirubin, cholesterol, triglycerides



- CAN progress to cirrhosis and end stage liver disease !!!! ****

cirrhosis

injury & death of heptocytes


--> excessive fibrosis



increased resistance to bloodflow thru liver


- portal hypertension



varices to relieve pressure


--> esophagus , umbilicus, rectum



ascites



splenomaegaly



encephalopathy



decreased albumin production

--> decreased oncotic pressure



--> increased hydrostatic pressure

major cause of mortality in end stage liver disease

bacterial infections... because decreased neutrophil activity

extra-oral features suggestive of advanced alcohol use

- attention/ memory deficits


- spider angiomas


- peripheral edema


- ascites


- palmar erythema


- ecchymoses + petechiea


- jaundice


- bilateral enlarged patorid gland enlargement

- attention/ memory deficits


- spider angiomas


- peripheral edema


- ascites


- palmar erythema


- ecchymoses + petechiea


- jaundice


- bilateral enlarged patorid gland enlargement

extra-oral features suggestive of advanced alcohol use

intra-oral features suggestive of advanced liver disease

- parotid gland involvement


- glossitis


- angular chelitis


- gingival bleeding


- intraoral petechiea + ecchymoses


- jaundiced mucosa


- xerostomia


- candida infections


- lichen planus (hep c)

carriers of viral hepatitis

NO infection control modifications necessary



cannot refuse care bc of high viral load

pt w acute symptomatic hepatitis

avoid elective care unless patient is clinically recovered

medical consult for pt with fibrosis/cirhois of liver

- CBC w differential


- platelet count


- INR + PTT


- liver function tests

what do liver functions tests measure?

measure biosynthetic function



tests measuring detoxification and excretory fxn = ALT, AST, LDH, alkaline phosphatase, bilirubin, albumin

primary liver enzymes

- AST, ALT, LDH, alkaline phosphatase


- present in liver cells


- hepatocytes (the enzymes show up in the blood)



--> increase indicates primary liver disease (destruction of liver cells)

increase of primary liver enzymes

- AST, ALT, LDH, alkaline phosphatase


- present in liver cells


- hepatocytes (the enzymes show up in the blood)


 


--> increase indicates primary liver disease (destruction of liver cells)

- AST, ALT, LDH, alkaline phosphatase


- present in liver cells


- hepatocytes (the enzymes show up in the blood)



--> increase indicates primary liver disease (destruction of liver cells)

child-pugh scoring

Child-pugh class a

child-pugh class B

when would you decrease dose or avoid drugs with a pt with liver fibrosis/cirrhosis ?

when one or more is present:


- aminotransferase levels are ≥ 4 times normal


- serum bilirubin is ≥ 35 µm/1 or 2mg/dl


- serum albumin levels are ≤ 35g/l

when one or more is present:


- aminotransferase levels are ≥ 4 times normal


- serum bilirubin is ≥ 35 µm/1 or 2mg/dl


- serum albumin levels are ≤ 35g/l

you decrease dose or avoid drugs with a pt with liver fibrosis/cirrhosis

in pts with liver disease... what analgesics would you AVOID?

AVOID


- ibuprofen


- aspirin



DECREASE dose


- acetaminophenen (always <4g/day in divided doses.... <2g/day in cirrhosis/heavy alcohol users)


- codeine (7.5mg q8h)


- meperidine

in pts with liver disease... what analgesics would you DECREASE DOSE?

AVOID


- ibuprofen


- aspirin



DECREASE dose


- acetaminophenen (always <4g/day in divided doses.... <2g/day in cirrhosis/heavy alcohol users)


- codeine (7.5mg q8h)


- meperidine

ibuprofen for pts with cirrhosis of liver

AVOID


- ibuprofen


- aspirin



DECREASE dose


- acetaminophenen (always <4g/day in divided doses.... <2g/day in cirrhosis/heavy alcohol users)


- codeine (7.5mg q8h)


- meperidine

acetaminophen for pts with cirrohis of liver

AVOID


- ibuprofen


- aspirin



DECREASE dose


- acetaminophenen (always <4g/day in divided doses.... <2g/day in cirrhosis/heavy alcohol users)


- codeine (7.5mg q8h)


- meperidine

in pts with liver disease... what DRUGS would you AVOID?

AVOID these antifungals


- ketoconazole


- fluconazole



AVOID these antibiotics


- tetracycline


- metronidazole


- vancomycin


- azithromycin/claritromycin/ erythromycin



REDUCED dose


- diazepam


- barbituates

in pts with liver disease... what DRUGS would you LOWER DOSE?

AVOID these antifungals


- ketoconazole


- fluconazole



AVOID these antibiotics


- tetracycline


- metronidazole


- vancomycin


- azithromycin/claritromycin/ erythromycin



REDUCED dose


- diazepam


- barbituates

azoles in pts with cirrhosis of liver

AVOID these antifungals


- ketoconazole


- fluconazole



AVOID these antibiotics


- tetracycline


- metronidazole


- vancomycin


- azithromycin/claritromycin/ erythromycin



REDUCED dose


- diazepam


- barbituates

diazepam and barbituates in pts with liver cirrhosis

AVOID these antifungals


- ketoconazole


- fluconazole



AVOID these antibiotics


- tetracycline


- metronidazole


- vancomycin


- azithromycin/claritromycin/ erythromycin



REDUCED dose


- diazepam


- barbituates

antibiotics for pts with liver cirrhosis

AVOID these antifungals


- ketoconazole


- fluconazole



AVOID these antibiotics


- tetracycline


- metronidazole


- vancomycin


- azithromycin/claritromycin/ erythromycin



REDUCED dose


- diazepam


- barbituates




**PENICILLIN / AMOXICILLIN USUALLY SAFE

Euthyroid

Euthyroid


- Normal thyroid hormone levels



Hyperthyroidism (thyrotoxicosis)


- Increased production of thyroid hormone


- Excessive formation and secretion



Hypothyroidism


- primary = Decreased production of thyroid hormone


- secondary = Decreased secretion due pituitary not secreting TSH

Hyperthyroidism (thyrotoxicosis)

Euthyroid


- Normal thyroid hormone levels



Hyperthyroidism (thyrotoxicosis)


- Increased production of thyroid hormone


- Excessive formation and secretion



Hypothyroidism


- primary = Decreased production of thyroid hormone


- secondary = Decreased secretion due pituitary not secreting TSH

Hypothyroidism

Euthyroid


- Normal thyroid hormone levels



Hyperthyroidism (thyrotoxicosis)


- Increased production of thyroid hormone


- Excessive formation and secretion



Hypothyroidism


- primary = Decreased production of thyroid hormone


- secondary = Decreased secretion due pituitary not secreting TSH

Lab Findings and Medical Treatment in pt w/ HYPO-throidism

- INCREASED TSH


- DECREASED T3/T4

Lab Findings and Medical Treatment in pt w/ HYPER-throidism

- DECREASED TSH


- INCREASED T3/T4

Causes of Hypothyroidism

***Autoimmune


--> Hashimoto’s disease



- secondary to treatment for hyperthyroidism


----> Surgical removal of gland


---->Radioactive iodine thyroid gland ablation



- External irradiation


- Drug-­‐induced


---> Lithium, sulfonamides


- Pituitary and hypothalamic disease

Hypothyroidism

- In utero-­cretinism
- In adults
--> Most severe form-­‐myxedema
- Slowing of metabolic processes


- Mental slowness, decreased concentration, dementia
- Dry rough skin, brittle hair
- Enlarged tongue
- Weight gain, cold intolerance
- Decreased cardiac output
- Bradycardia, hypotension
- Decreased respiratory drive


- constipation

myxedema coma

- Patient with poorly controlled hypothyroidism



Certain factors may suddenly trigger


- Drugs


- Par1cularly sedatives, narcotics, anesthesia, lithium (Eskalith, Lithobid), and amiodarone


- Infections


- Trauma


- Heart failure


- Gastrointestinal bleeding


- Hypothermia/Cold


- Failing to take thyroid medications as prescribed.




**LIFE-THREATENING EMERGENCY***

symptoms of severea myxedema coma

- HYPOthermia


- HYPOventilation


- HYPOxia


- HYPOtension



--> seek medical aid, cover to conserve heat, Hydrocortisone 100-300mg, CPR

autoimune cause of HYPO-thyroidism

hashimotos !!!!



autoimmune cause of HYPER-thyroidism is Graves disease

autoimmune cause of HYPER-thyroidism

Graves disease



autoimune cause of HYPO-thyroidism is hashimotos

causes of HYPER-thyroidism

***Autoimmune


–Grave’s disease



- Adenoma


- Multinodular goiter


- Subacute thyroiditis


- Iodine-­induced hyperthroidism


- Excessive pituitary thyroid stimulating hormone (TSH)

most COMMON cause of hyperhyroidism

Grave's disease

Grave's disease

- most frequent cause of hyperthyroidism


- toxic diffuse goiter


- exophthalmos


--> protrusion of the globe of the eye, proptosis and restriction of eye movement

symptoms of HYPER-thyroidism

- Acceleration of metabolic processes
- Nervousness, insomnia, tremors, irritability, agitation
- Warm, moist skin; fine, thin hair; excessive perspiration
- Weight loss, heat intolerance
- Palpitations, atrial fibrillation, tachycardia
- Dyspnea
- Diarrhea


thyroid storm (thyrotoxic crisis)

- life- threatening


- can be precipitated by


---> stress, infection, vigorous thyroid gland palpation



clinical signs:


- elevated body temp; marked tachycardia; extreme restlessness; agitation


- tremor; mental confusion


- coma + death if not promptly treated

clinical signs of thyroid storm

- life- threatening


- can be precipitated by


---> stress, infection, vigorous thyroid gland palpation



clinical signs:


- elevated body temp; marked tachycardia; extreme restlessness; agitation


- tremor; mental confusion


- coma + death if not promptly treated

how to treat a hyperthyroid crisis

•    Begins emergency therapy and get immediate medical assistance

•    Cool patient with cold towels/ice packs

•    Hydrocortisone (100-­‐300 mg IM or IV)

•    IV infusion of glucose (D50W)

•    Monitor vital signs...

• Begins emergency therapy and get immediate medical assistance
• Cool patient with cold towels/ice packs
• Hydrocortisone (100-­‐300 mg IM or IV)
• IV infusion of glucose (D50W)
• Monitor vital signs
• Initiate CPR as needed


HYPO vs HYPER thyrodism

cold intolerance / heat intolerance

respitory signs + symptoms of pts with HYPO vs HYPER thyroidism

dental management of HYPO-thyroidism

• Assessment of clinical status
• Underlying cause and stability
• Medications



Untreated/poorly treated
– Avoid
–-> Surgical procedures
–-> CNS depressants
–-> Oral infection



• Recognition of myxedema coma
• Good control
– Normal procedures and management
– No special precautions

avoid for hypo-throidism pts

• Assessment of clinical status
• Underlying cause and stability
• Medications



Untreated/poorly treated
– Avoid
–-> Surgical procedures
–-> CNS depressants
–-> Oral infection



• Recognition of myxedema coma
• Good control
– Normal procedures and management
– No special precautions

avoid for HYPER-throidism pts

• Underlying cause and stability
• Medications



Untreated/poorly treated: Avoid


--> Surgical procedures
--> Epinephrine and other pressor amines
--> Acute oral infection



• Recognition of thyrotoxic crisis
• Good control
– Normal procedures and management
– No special precautions

adrenal medula produces

- epinephrine


- norepinephrine


- dopamine

what produces:



- epinephrine


- norepinephrine


- dopamine

adrenal medula

cortisol

• Maintain blood pressure and cardiovascular function
Slow the immune system's inflammatory response
• Helps regulate the metabolism of proteins, carbohydrates, and fats
• Helps regulate insulin and glucose metabolism


commonly prescribed replacement steroid equivalents

hydrocortisone is EQUAL in potency to cortisol



prednisone is 4x more potent !!!!

prednisone vs. hydrocortisone

hydrocortisone is EQUAL in potency to cortisol



prednisone is 4x more potent !!!!

cortisol peaks

Normal cortisol production
– Peaks in the early morning hours (6 am–8 am)
– Second lower peak in evening



In an adult who is not experiencing stress
– Average amount of cortisol is 20-­‐30 mg/day
– Equivalent to approx. 5-­‐7 mg of prednisone



During stress
– Cortisol production increases
– 50-­‐200 mg/day


Disorders of Adrenal Cortex

• Primary Adrenal Cortical Insufficiency
– Addison’s Disease



• Secondary Adrenal Insufficiency
– Hypopituitarism (↓release of ACTH)
– Chronic Steroid Therapy



• Adrenal Cortical Hyperactivity
– Cushing’s Disease


----> Pituitary tumor causing chronic glucocorticoid excess


– Cushing’s Syndrome


----> Chronic administration of corticosteroids to tx immunological and inflammatory disorders


cushing's syndrome vs disease

– Cushing’s Disease


----> Pituitary tumor causing chronic glucocorticoid excess



– Cushing’s Syndrome


----> Chronic administration of corticosteroids to tx immunological and inflammatory disorders

Addison's disease (primary adrenal insufficiency)

• Deficiency of aldosterone and cortisol.
– Weakness
– Fatigue
– Hypotension
– Anorexia and weight loss
– Abnormal pigmentation of the skin and mucous membranes



*** Higher risk of adrenal crisis if stressed


dental management of HYPER-thyroidism

• Underlying cause and stability
• Medications



Untreated/poorly treated: Avoid


--> Surgical procedures
--> Epinephrine and other pressor amines
--> Acute oral infection



• Recognition of thyrotoxic crisis
• Good control
– Normal procedures and management
– No special precautions

medical management of: Addison's disease (primary adrenal insufficiency)

• Glucocorticoid replacement
– Levels that correspond to normal physiologic output of the adrenal cortex
– About 25 to 30 mg cortisol per day
--> Hydrocortisone 30 mg/day (20mg in AM and 10 in evening)
--> Prednisone 5-­‐7 mg/day
--> Dexamethasone 0.75 mg/day



• Mineralocorticoid replacement


secondary adrenal insufficiency

• Most common from chronic corticosteroid administration
• Partial insufficiency limited to glucocorticoids
Usually does not produce any symptoms
– Unless the patient is significantly stressed AND does not have adequate circulating cortisol to cope with the stress.
• Adrenal crisis rare


cushing's syndrome (HYPER-adrenalism)

• A “Cushingoid” patient dislplays
– Weight gain
– Round or moon-­‐shaped facies
– “Buffalo hump" on the back
– Acne
– Hypertension
– Heart failure
– Osteoporosis and bone fractures
– Diabetes mellitus
– Impaired and delayed wound healing


– Weight gain
– Round or moon-­‐shaped facies
– “Buffalo hump" on the back
– Acne
– Hypertension
– Heart failure
– Osteoporosis and bone fractures
– Diabetes mellitus
– Impaired and delayed wound healing


cushing's syndrome (HYPER-adrenalism)

problems associated with adverse effects of chronic steroid use

- immunosuppression


- hypertension


- osteoporosis


- hypergylcemia


- muscle weakness


- GI ulcers

Which patients are at risk for adrenal insufficiency?

• Addison’s Disease (primary AI)
High risk
– Unable to synthesize cortisol and aldosterone in response to stress
– Rapid shock and circulatory collapse




**(LOW risk for exogenous steroid use .. secondary)

Adrenal Crisis

• More common in primary adrenal insufficiency
• Life-­‐threatening
• Follows physiologically stressful event



• Evolves slowly over a few hours
– GI-­‐nausea, vomiting, diarrhea, cramps
– Hypotension
– Weak pulse
– Profuse sweating
– Weakness and fatigue
– Headaches
– Dyspnea and cyanosis
– Myalgias and arthralgia


Tx of Adrenal Crisis

• STAT 100-­‐mg hydrocortisone bolus—and intravenous fluid and electrolyte replacement to restore the blood pressure.


• After the initial treatment
– 100 mg of hydrocortisone is administered slowly intravenously every six to eight hours during the first 24 hours
– Fluid replacement, vasopressors and correction of hypoglycemia, if needed


dental management for pts taking systemic corticosteroids

• For diagnostic, all restorative, endodontic and periodontal and minor oral surgery procedures
– Have patient take usual daily dose
– Perform oral procedure in morning
– Take blood pressure before and after procedure
– Stress reduction measures



· For major oral surgery (multiple extractions, impactions, jaw surgery) or sedation
– Consult with physician
– Implement steroid supplementation protocol

supplemental steroids for dental tx?

NO routine, non-surgival dental procedures warrant supplemental steroids before/during/after the operative period



however... for minor oral surgery (few extractions... biopsy.. single tooth implant, minor perio surgery)


--> 25mg of hydrocortisone (5-6mg prednisone) on the day of surgery



--> for moderate , target is 50mg hydrocortison


(multiple extractions, bony impactions, mult implants)


--> MAJOR (surgery > 1 hour... genanesthesia)


= 50-100mg hydrocortisone + 1 day post-op

surgery for a pt on steroids

NO routine, non-surgival dental procedures warrant supplemental steroids before/during/after the operative period



however... for minor oral surgery (few extractions... biopsy.. single tooth implant, minor perio surgery)


--> 25mg of hydrocortisone (5-6mg prednisone) on the day of surgery



--> for moderate , target is 50mg hydrocortison


(multiple extractions, bony impactions, mult implants)


--> MAJOR (surgery > 1 hour... genanesthesia)


= 50-100mg hydrocortisone + 1 day post-op

major surgery for pt on steroids

NO routine, non-surgival dental procedures warrant supplemental steroids before/during/after the operative period



however... for minor oral surgery (few extractions... biopsy.. single tooth implant, minor perio surgery)


--> 25mg of hydrocortisone (5-6mg prednisone) on the day of surgery



--> for moderate , target is 50mg hydrocortison


(multiple extractions, bony impactions, mult implants)


--> MAJOR (surgery > 1 hour... genanesthesia)


= 50-100mg hydrocortisone + 1 day post-op

moderate surgery for pt on steroids

NO routine, non-surgival dental procedures warrant supplemental steroids before/during/after the operative period



however... for minor oral surgery (few extractions... biopsy.. single tooth implant, minor perio surgery)


--> 25mg of hydrocortisone (5-6mg prednisone) on the day of surgery



--> for moderate , target is 50mg hydrocortison


(multiple extractions, bony impactions, mult implants)


--> MAJOR (surgery > 1 hour... genanesthesia)


= 50-100mg hydrocortisone + 1 day post-op

acute adrenal crisis

- position patient semi-reclining with legs elevated


- call 911


-administer oxygen and monitor blood pressure


- administer 100mg SoluCortef (hydrocortisone)


- transport to medical facility

mortality rate in individuals with diabetes

mortality rate is DOUBLED in individuals with diabetes


---> increased risk of cardiovascular mortality

why is muscle unable to use glucose in type 1 diabetes?

type 1 --> muscle unable to use glucose due to low insulin



type 2 --> muscle unable to use glucose due to insulin resistance

why is muscle unable to use glucose in type 2 diabetes?

type 1 --> muscle unable to use glucose due to low insulin



type 2 --> muscle unable to use glucose due to insulin resistance

type 1 vs type 2 diabetes

normal fasting plasma glucose

normal = < 100


pre-diabetes = between 100 & 125


diabetes = >126

diabetes fasting blood glucose

normal = < 100


pre-diabetes = between 100 & 125


diabetes = >126

2 hour plasma glucose challenge

normal: < 126


impaired: betw 140-200


diabetes: > 200

basic levels of glycoslated hemoglobin

used to determine how well controleld pt is



<6 --> very excellent


9 --> fair


>12 --> very poor

what does Metformin do?

it is a biguanide


--> enhances liver and muscle insulin sensitivity

symptoms of HYEPR-glycemia

- going to bathroom a lot


- very thirsty


- feeling tired


- feeling weak


- blurry vision


- feeling hungry (even after a meal)

symptoms of HYPO-gylcemia

- shakiness


- dizziness


- nervousness


- sweating a lot***


- hunger


- headache


- pale face


- clumsiness


- confusion


- trouble paying attention


- tingling around the mouth


- passing out (fainting)

what drugs does a pt take that could most commonly cause HYPO-glycemia?

- MOST likely with insulin


- more likely with sulfonyureas


- uncommon with other meds... esp metformin

good glycemic control

FBS: < 110mg/dl


HbA1c: <7%

moderate glycemic control

FBS: < 2000mg/dl


HbA1c: 7-8.5%

poor glycemic control

FBS: >200mg/dl


HbA1c >8.5%

dental management for diabetic pt

- confirm pt has taken usual insulin dosage or oral hypoglycemic AND eaten normal meal


(less critical with metformin)



- avoid scheduling during meal time

when might signs of HYPO-glycemis become blunted/absent?

if a pt is taking beta-blockers !!!



--> diaphoresis (sweating) actually increases

best and worse case scenarios of dental management of a diabetic

BEST = pt took meds and ate... (blood sugar should be close to normal)



WORST = took meds but did NOT eat (blood sugar may drop a LOT)



OK --> pt ate but did NOT take meds



SO-SO --> didnt take meds OR eat

if a pt starts experiencing symptoms of hypoglycemia

- administer 15gms sugar source EVEN IF YOU ARE NOT SURE IT SI HYPOGLYCEMIA !!!!



NEVER GIVE A PT INSULIN !!!!!!!!!!!!!!

diabetes and periodontal disease

periodontal disease is THE MOST PREVALENT oral complication of diabetics

how does poor glycemic control affect salivary flow and crevcular fluid?

DECREASES salivary flow and INCREASES glucose concentration in crevicular fluid

diabetes and caries

- poorly controlled have increased glucose in salivary secretion


--> INCREASED root caries



well-controlled have lower intake of carbs


--> may have diminished caries rate

diabetes and dental pulp

- GREATER prevalence of periapical lesions in diabetics than in nondiabetics


- b/c the dental pulp has limited or NO collateral circulation, it is more prone to infection



in pts with good glycemic control..


--> periapical and other lesions heal as readily as in non-diabetics

diabetes and xerostomia

- 80% of poorly controlled diabetics


- decreased parotid flow rates


- INCREASE in candidiasis


--> especially with dentures


--> use azole antifungals with care in pts on TZDs


- INCREASED oral burning and taste disturbances

what is the most common cause of renal disease?

DIABETES !!!!



diabetes --> hypertension --> renal failure

most common causes of chronic renal failure

- diabetic nephropathy


- nephrosclerosis secondary to HTN

co-morbitities of patients with renal disease

- 100% have HTN


- 75 % have diabetes


- 60% have coronary arery disease


34% have ischemic heart disease


- 25% have congestive heart failure

symptoms of renal failure

ASYMPTOMATIC until about 50% of the nephrons are lost


--> then the compensatory mechanisms are overwhelmed

symptoms of renal insufficiency

- headaches


- decreased ability to concentrate urine


- polyuria --> oliguria


- INCREASED BUN and serum creatinine


- edema


- mild anemia


- INCREASED BP


- weakness + fatigue


- GFR progressively decreases from 90 to 30 ml/min

symptoms of end stage renal failure

- neurological weakness/fatigue & confusion


- increased BP


- pitting edema; periorbital edema, pericarditis


- SOB, depressed cough, thick sputum


- ammonia odor to breath; metallic taste, anorexia


- withdrawn; depression


- anemia; bleeding tendencies


- dry flaky skin; pruritis, ecchymosis; purpura

laboratory findings in renal disease

- HYPER-kalemia


- acidosis


- HYPO-calcemia


- HYPER-phosphatemia


- HYPER + HYPO - natremia


- moderately severe normochromic-normocytic anemia


- leukocyte and platelet destruction


- coagulopathies

what kind of anemia would a pt with renal disease have

- HYPER-kalemia


- acidosis


- HYPO-calcemia


- HYPER-phosphatemia


- HYPER + HYPO - natremia


- moderately severe normochromic-normocytic anemia


- leukocyte and platelet destruction


- coagulopathies

azotemia

- buildup of blood urea nitrogen compounds (mainly urea)


- acids accumulate --> metabolic acidosis


- ammonia retention

normal GFR

normal = 90-120 mL/min


CKD 2 = 60-90


CKD 3 = 30-60


CKD 4 = 15-30


CKD 5 = <15

uremia leads to:

- HTN


- anemia


- bleeding problems


- electrolyte and fluid imbalance


- malnutrition and diarrhea


- mental slowness, psychosis, convulsions


- altered drug metabolism

complications of renal failure

- DECREASED glomerular perfusion


--> activates renin-angiotension system


--> increases BP



fluid shifts related to sodium/water shifts


- fluid volume overload


- mild edema to life-threatening pulmonary edema


--> secondary hypertension and CHF

oral findings in pts with renal disease

- pallor of oral mucosa


- bad taste/halitosis --> b/c urea in saliva


- petechiae and exxhymosis


- mucosal / gingival hemorrhang


- xerostomia / candidiasis


- parotid inflammation and enlargement


- NUG and periodontitis


- radiographic triad of: loss of lamina dura; ground glass appearance of bone; RL lesions

dental findings in pts with renal disease

tooth erosion


--> secondary to vomitting



decreased occlusal/interproximal caries


--> increased urea



increased cervical caries


--> fluid restrictions and xerostomia